rail_id	run_acc	study_acc	sample_acc	experiment_acc	submission_acc	submission_center	submission_lab	study_title	study_abstract	study_description	experiment_title	design_description	sample_description	library_name	library_strategy	library_source	library_selection	library_layout	paired_nominal_length	paired_nominal_stdev	library_construction_protocol	platform_model	sample_attributes	experiment_attributes	spot_length	sample_name	sample_title	sample_bases	sample_spots	run_published	size	run_total_bases	run_total_spots	num_reads	num_spots	read_info	run_alias	run_center_name	run_broker_name	run_center	MESA	pubmed_id	aligned_reads%.chrm	aligned_reads%.chrx	aligned_reads%.chry	bc_auc.all_reads_all_bases	bc_auc.all_reads_annotated_bases	bc_auc.unique_reads_all_bases	bc_auc.unique_reads_annotated_bases	bc_auc.all_%	bc_auc.unique_%	bc_frag.count	bc_frag.kallisto_count	bc_frag.kallisto_mean_length	bc_frag.mean_length	bc_frag.mode_length	bc_frag.mode_length_count	exon_fc.all_%	exon_fc.unique_%	exon_fc_count_all.total	exon_fc_count_all.assigned	exon_fc_count_unique.total	exon_fc_count_unique.assigned	gene_fc.all_%	gene_fc.unique_%	gene_fc_count_all.total	gene_fc_count_all.assigned	gene_fc_count_unique.total	gene_fc_count_unique.assigned	intron_sum	Iintron_sum_%	star.%_of_chimeric_reads	star.%_of_chimeric_reads2	star.%_of_reads_mapped_to_multiple_loci	star.%_of_reads_mapped_to_multiple_loci2	star.%_of_reads_mapped_to_too_many_loci	star.%_of_reads_mapped_to_too_many_loci2	star.%_of_reads_unmapped:_other	star.%_of_reads_unmapped:_other2	star.%_of_reads_unmapped:_too_many_mismatches	star.%_of_reads_unmapped:_too_many_mismatches2	star.%_of_reads_unmapped:_too_short	star.%_of_reads_unmapped:_too_short2	star.all_mapped_reads	star.all_mapped_reads2	star.average_input_read_length	star.average_input_read_length2	star.average_mapped_length	star.average_mapped_length2	star.deletion_average_length	star.deletion_average_length2	star.deletion_rate_per_base	star.deletion_rate_per_base2	star.insertion_average_length	star.insertion_average_length2	star.insertion_rate_per_base	star.insertion_rate_per_base2	star.mapping_speed,_million_of_reads_per_hour	star.mapping_speed,_million_of_reads_per_hour2	star.mismatch_rate_per_base,_%	star.mismatch_rate_per_base,_%2	star.number_of_chimeric_reads	star.number_of_chimeric_reads2	star.number_of_input_reads	star.number_of_input_reads2	star.number_of_reads_mapped_to_multiple_loci	star.number_of_reads_mapped_to_multiple_loci2	star.number_of_reads_mapped_to_too_many_loci	star.number_of_reads_mapped_to_too_many_loci2	star.number_of_reads_unmapped:_other	star.number_of_reads_unmapped:_other2	star.number_of_reads_unmapped:_too_many_mismatches	star.number_of_reads_unmapped:_too_many_mismatches2	star.number_of_reads_unmapped:_too_short	star.number_of_reads_unmapped:_too_short2	star.number_of_splices:_at/ac	star.number_of_splices:_at/ac2	star.number_of_splices:_annotated_(sjdb)	star.number_of_splices:_annotated_(sjdb)2	star.number_of_splices:_gc/ag	star.number_of_splices:_gc/ag2	star.number_of_splices:_gt/ag	star.number_of_splices:_gt/ag2	star.number_of_splices:_non-canonical	star.number_of_splices:_non-canonical2	star.number_of_splices:_total	star.number_of_splices:_total2	star.uniquely_mapped_reads_%	star.uniquely_mapped_reads_%2	star.uniquely_mapped_reads_number	star.uniquely_mapped_reads_number2	junction_count	junction_coverage	junction_avg_coverage	star.number_of_input_reads_both	star.all_mapped_reads_both	star.number_of_chimeric_reads_both	star.number_of_reads_mapped_to_multiple_loci_both	star.number_of_reads_mapped_to_too_many_loci_both	star.number_of_reads_unmapped:_other_both	star.number_of_reads_unmapped:_too_many_mismatches_both	star.number_of_reads_unmapped:_too_short_both	star.uniquely_mapped_reads_number_both	star.%_mapped_reads_both	star.%_chimeric_reads_both	star.%_reads_mapped_to_multiple_loci_both	star.%_reads_mapped_to_too_many_loci_both	star.%_reads_unmapped:_other_both	star.%_reads_unmapped:_too_many_mismatches_both	star.%_reads_unmapped:_too_short_both	star.uniquely_mapped_reads_%_both
1458334	SRR1975409	SRP057202	SRS910994	SRX996672	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658706: RQ_CSD1; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658706		GSM1658706	RQ_CSD1	418786160	24634480	2016-04-14 16:08:07	345942445	418786160	24634480	1	24634480	index:0,count:24634480,average:17,stdev:0	GSM1658706_r1	GEO					2.45	4.53	0.11	371351400	297181784	146800964	144008624	80.03	98.1	0	0	0	0	0	0	34.92	88.66	55241581	7661073	55241581	7661073	56.76	84.68	55241581	12450814	55241581	7317004	70720060	19.04	0.00	0	53.97	0	6.11	0	4.84	0	0.00	0	0.00	0	21936348	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	509.68	0	0.00	0	0	0	24634480	0	13295598	0	1504852	0	1193280	0	0	0	0	0	0	0	0	0	0	0	24	0	0	0	24	0	35.08	0	8640750	0	0	0	-nan	24634480.0	21936348.0	0.0	13295598.0	1504852.0	1193280.0	0.0	0.0	8640750.0	89.0	0.0	54.0	6.1	4.8	0.0	0.0	35.1
1458446	SRR1975410	SRP057202	SRS910993	SRX996673	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658707: RQ_CSD2; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658707		GSM1658707	RQ_CSD2	395551563	23267739	2016-04-14 16:08:07	327399685	395551563	23267739	1	23267739	index:0,count:23267739,average:17,stdev:0	GSM1658707_r1	GEO					2.43	4.53	0.14	353960127	283526688	140179924	137488864	80.1	98.08	0	0	0	0	0	0	35.0	88.69	52508412	7318003	52508412	7318003	56.74	84.64	52508412	11864049	52508412	6984125	67625426	19.11	0.00	0	54.41	0	5.99	0	4.14	0	0.00	0	0.00	0	20910827	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	594.07	0	0.00	0	0	0	23267739	0	12659745	0	1393661	0	963251	0	0	0	0	0	0	0	0	0	0	0	36	0	0	0	36	0	35.46	0	8251082	0	0	0	-nan	23267739.0	20910827.0	0.0	12659745.0	1393661.0	963251.0	0.0	0.0	8251082.0	89.9	0.0	54.4	6.0	4.1	0.0	0.0	35.5
1458462	SRR1975411	SRP057202	SRS910992	SRX996674	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658708: RQ_CSD3; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658708		GSM1658708	RQ_CSD3	236851820	13932460	2016-04-14 16:08:07	197440237	236851820	13932460	1	13932460	index:0,count:13932460,average:17,stdev:0	GSM1658708_r1	GEO					2.28	4.54	0.11	211753593	168843955	84842587	83502875	79.74	98.42	0	0	0	0	0	0	35.57	89.09	31314142	4448831	31314142	4448831	56.19	84.91	31314142	7028708	31314142	4240207	40675028	19.21	0.00	0	53.93	0	5.98	0	4.25	0	0.00	0	0.00	0	12508302	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	522.47	0	0.00	0	0	0	13932460	0	7514472	0	832576	0	591582	0	0	0	0	0	0	0	0	0	0	0	16	0	0	0	16	0	35.84	0	4993830	0	0	0	-nan	13932460.0	12508302.0	0.0	7514472.0	832576.0	591582.0	0.0	0.0	4993830.0	89.8	0.0	53.9	6.0	4.2	0.0	0.0	35.8
1458478	SRR1975412	SRP057202	SRS910991	SRX996675	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658709: RQ_CSD4; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658709		GSM1658709	RQ_CSD4	371977153	21881009	2016-04-14 16:08:07	303040886	371977153	21881009	1	21881009	index:0,count:21881009,average:17,stdev:0	GSM1658709_r1	GEO					3.62	4.52	0.11	335446604	270886829	135324763	132837691	80.75	98.16	0	0	0	0	0	0	35.76	88.94	48837024	7084079	48837024	7084079	58.07	85.12	48837024	11504448	48837024	6779530	62459682	18.62	0.00	0	54.13	0	5.80	0	3.66	0	0.00	0	0.00	0	19810262	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	550.85	0	0.00	0	0	0	21881009	0	11845223	0	1269492	0	801255	0	0	0	0	0	0	0	0	0	0	0	34	0	0	0	34	0	36.40	0	7965039	0	0	0	-nan	21881009.0	19810262.0	0.0	11845223.0	1269492.0	801255.0	0.0	0.0	7965039.0	90.5	0.0	54.1	5.8	3.7	0.0	0.0	36.4
1458494	SRR1975413	SRP057202	SRS910990	SRX996676	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658710: RQ_CSD5; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658710		GSM1658710	RQ_CSD5	159050997	9355941	2016-04-14 16:08:07	133414334	159050997	9355941	1	9355941	index:0,count:9355941,average:17,stdev:0	GSM1658710_r1	GEO					2.66	4.72	0.12	142835343	113475898	58062275	56091594	79.45	96.61	0	0	0	0	0	0	34.83	86.12	20982603	2943703	20982603	2943703	55.6	82.47	20982603	4699209	20982603	2819161	28304526	19.82	0.00	0	53.81	0	5.64	0	4.02	0	0.00	0	0.00	0	8452401	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	518.18	0	0.00	0	0	0	9355941	0	5034107	0	527667	0	375873	0	0	0	0	0	0	0	0	0	0	0	21	0	0	0	21	0	36.54	0	3418294	0	0	0	-nan	9355941.0	8452401.0	0.0	5034107.0	527667.0	375873.0	0.0	0.0	3418294.0	90.3	0.0	53.8	5.6	4.0	0.0	0.0	36.5
1458508	SRR1975414	SRP057202	SRS910990	SRX996676	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658710: RQ_CSD5; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658710		GSM1658710	RQ_CSD5	39547794	1797627	2016-04-14 16:08:07	31176765	39547794	1797627	1	1797627	index:0,count:1797627,average:22,stdev:0	GSM1658710_r2	GEO					3.72	4.6	0.12	36227704	32078905	25727188	24952928	88.55	96.99	0	0	0	0	0	0	60.19	86.36	2851310	1038322	2851310	1038322	69.57	82.1	2851310	1200115	2851310	987095	4301484	11.87	0.00	0	29.08	0	1.90	0	2.12	0	0.00	0	0.01	0	1725081	0	22	0	21.40	0	0.00	0	0.00	0	0.00	0	0.00	0	165.93	0	0.24	0	0	0	1797627	0	522801	0	34235	0	38067	0	0	0	244	0	0	0	0	0	24	0	2941	0	0	0	2965	0	66.88	0	1202280	0	0	0	-nan	1797627.0	1725081.0	0.0	522801.0	34235.0	38067.0	0.0	244.0	1202280.0	96.0	0.0	29.1	1.9	2.1	0.0	0.0	66.9
1458523	SRR1975415	SRP057202	SRS910989	SRX996677	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658711: RQ_CSD6; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658711		GSM1658711	RQ_CSD6	937749318	42624969	2016-04-14 16:08:07	757017521	937749318	42624969	1	42624969	index:0,count:42624969,average:22,stdev:0	GSM1658711_r1	GEO					3.22	4.5	0.17	846886223	721698978	577063928	545214710	85.22	94.48	0	0	0	0	0	0	54.78	82.49	72047968	22404144	72047968	22404144	63.76	78.39	72047968	26077812	72047968	21292663	120614464	14.24	0.00	0	32.24	0	2.14	0	1.88	0	0.00	0	0.02	0	40901384	0	22	0	21.25	0	1.00	0	0.00	0	1.00	0	0.00	0	204.60	0	0.22	0	0	0	42624969	0	13740205	0	912433	0	800608	0	0	0	10544	0	0	0	0	0	295	0	104476	0	0	0	104771	0	63.72	0	27161179	0	0	0	-nan	42624969.0	40901384.0	0.0	13740205.0	912433.0	800608.0	0.0	10544.0	27161179.0	96.0	0.0	32.2	2.1	1.9	0.0	0.0	63.7
1458537	SRR1975416	SRP057202	SRS910988	SRX996678	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658712: RQ_SHAM1; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658712		GSM1658712	RQ_SHAM1	213566869	12562757	2016-04-14 16:08:07	177918874	213566869	12562757	1	12562757	index:0,count:12562757,average:17,stdev:0	GSM1658712_r1	GEO					2.57	4.48	0.1	190804558	153039490	76340506	74825264	80.21	98.02	0	0	0	0	0	0	35.23	88.42	28176357	3973234	28176357	3973234	56.96	84.5	28176357	6423516	28176357	3797125	36475764	19.12	0.00	0	54.00	0	5.90	0	4.33	0	0.00	0	0.00	0	11277109	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	595.08	0	0.00	0	0	0	12562757	0	6783574	0	741184	0	544464	0	0	0	0	0	0	0	0	0	0	0	19	0	0	0	19	0	35.77	0	4493535	0	0	0	-nan	12562757.0	11277109.0	0.0	6783574.0	741184.0	544464.0	0.0	0.0	4493535.0	89.8	0.0	54.0	5.9	4.3	0.0	0.0	35.8
1458554	SRR1975417	SRP057202	SRS910987	SRX996679	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658713: RQ_SHAM2; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658713		GSM1658713	RQ_SHAM2	248625374	14625022	2016-04-14 16:08:07	204486075	248625374	14625022	1	14625022	index:0,count:14625022,average:17,stdev:0	GSM1658713_r1	GEO					2.5	4.45	0.1	223486488	180061795	90874144	90045560	80.57	99.09	0	0	0	0	0	0	36.6	90.27	32515308	4827835	32515308	4827835	57.8	86.06	32515308	7624274	32515308	4602552	41186395	18.43	0.00	0	53.62	0	5.58	0	4.23	0	0.00	0	0.00	0	13189705	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	548.44	0	0.00	0	0	0	14625022	0	7841657	0	816801	0	618516	0	0	0	0	0	0	0	0	0	0	0	12	0	0	0	12	0	36.57	0	5348048	0	0	0	-nan	14625022.0	13189705.0	0.0	7841657.0	816801.0	618516.0	0.0	0.0	5348048.0	90.2	0.0	53.6	5.6	4.2	0.0	0.0	36.6
1458570	SRR1975418	SRP057202	SRS910985	SRX996680	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658714: RQ_SHAM3; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658714		GSM1658714	RQ_SHAM3	634676504	37333912	2016-04-14 16:08:07	530422298	634676504	37333912	1	37333912	index:0,count:37333912,average:17,stdev:0	GSM1658714_r1	GEO					2.88	4.68	0.14	542710514	415921664	206094685	192626425	76.64	93.47	0	0	0	0	0	0	30.44	80.88	85009025	9822435	85009025	9822435	50.65	77.36	85009025	16341793	85009025	9395006	120356698	22.18	0.00	0	53.90	0	6.44	0	7.14	0	0.00	0	0.00	0	32266704	0	17	0	16.97	0	0.00	0	0.00	0	0.00	0	0.00	0	610.92	0	0.00	0	0	0	37333912	0	20121631	0	2402747	0	2664461	0	0	0	0	0	0	0	0	0	0	0	76	0	0	0	76	0	32.53	0	12145073	0	0	0	-nan	37333912.0	32266704.0	0.0	20121631.0	2402747.0	2664461.0	0.0	0.0	12145073.0	86.4	0.0	53.9	6.4	7.1	0.0	0.0	32.5
1458585	SRR1975419	SRP057202	SRS910986	SRX996681	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658715: RQ_SHAM4; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658715		GSM1658715	RQ_SHAM4	485482158	28557774	2016-04-14 16:08:07	403772205	485482158	28557774	1	28557774	index:0,count:28557774,average:17,stdev:0	GSM1658715_r1	GEO					3.24	4.56	0.12	434424480	346929515	173583097	168757837	79.86	97.22	0	0	0	0	0	0	34.51	86.79	64503213	8869937	64503213	8869937	56.12	83.15	64503213	14424819	64503213	8497632	86202632	19.84	0.00	0	54.22	0	5.88	0	4.11	0	0.00	0	0.00	0	25703200	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	417.92	0	0.00	0	0	0	28557774	0	15483632	0	1680320	0	1174254	0	0	0	0	0	0	0	0	0	0	0	65	0	0	0	65	0	35.79	0	10219568	0	0	0	-nan	28557774.0	25703200.0	0.0	15483632.0	1680320.0	1174254.0	0.0	0.0	10219568.0	90.0	0.0	54.2	5.9	4.1	0.0	0.0	35.8
1458698	SRR1975420	SRP057202	SRS910984	SRX996682	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658716: RQ_SHAM5; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658716		GSM1658716	RQ_SHAM5	398992176	23470128	2016-04-14 16:08:07	335365565	398992176	23470128	1	23470128	index:0,count:23470128,average:17,stdev:0	GSM1658716_r1	GEO					1.79	4.96	0.13	352501088	276754899	143794244	136922003	78.51	95.22	0	0	0	0	0	0	33.91	83.79	52650677	7097646	52650677	7097646	53.93	80.19	52650677	11287356	52650677	6792721	71935485	20.41	0.00	0	53.08	0	4.93	0	5.90	0	0.00	0	0.00	0	20928363	0	17	0	16.98	0	0.00	0	0.00	0	0.00	0	0.00	0	524.80	0	0.00	0	0	0	23470128	0	12458083	0	1156682	0	1385083	0	0	0	0	0	0	0	0	0	0	0	30	0	0	0	30	0	36.09	0	8470280	0	0	0	-nan	23470128.0	20928363.0	0.0	12458083.0	1156682.0	1385083.0	0.0	0.0	8470280.0	89.2	0.0	53.1	4.9	5.9	0.0	0.0	36.1
1458714	SRR1975421	SRP057202	SRS910983	SRX996683	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658717: RQ_SHAM6; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;Homozygous R192Q CACNA1A Knock-in|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658717		GSM1658717	RQ_SHAM6	902604230	41027465	2016-04-14 16:08:07	689960910	902604230	41027465	1	41027465	index:0,count:41027465,average:22,stdev:0	GSM1658717_r1	GEO					3.64	4.42	0.15	826106207	721987198	587313480	562034798	87.4	95.7	0	0	0	0	0	0	59.28	85.12	66035726	23452734	66035726	23452734	68.22	80.99	66035726	26989695	66035726	22314892	99544279	12.05	0.00	0	29.27	0	1.88	0	1.67	0	0.00	0	0.02	0	39563354	0	22	0	21.32	0	1.00	0	0.00	0	1.00	0	0.00	0	234.44	0	0.16	0	0	0	41027465	0	12009826	0	771426	0	683831	0	0	0	8854	0	0	0	0	0	233	0	81000	0	0	0	81233	0	67.16	0	27553528	0	0	0	-nan	41027465.0	39563354.0	0.0	12009826.0	771426.0	683831.0	0.0	8854.0	27553528.0	96.4	0.0	29.3	1.9	1.7	0.0	0.0	67.2
1458730	SRR1975422	SRP057202	SRS910980	SRX996684	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658718: WT_CSD1; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658718		GSM1658718	WT_CSD1	309595024	18211472	2016-04-14 16:08:07	257182008	309595024	18211472	1	18211472	index:0,count:18211472,average:17,stdev:0	GSM1658718_r1	GEO					1.77	4.61	0.13	277353490	220736849	112777142	110986294	79.59	98.41	0	0	0	0	0	0	36.12	89.18	41111153	5919440	41111153	5919440	56.01	85.07	41111153	9179555	41111153	5647011	53511649	19.29	0.00	0	53.54	0	5.83	0	4.18	0	0.00	0	0.00	0	16388906	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	590.64	0	0.00	0	0	0	18211472	0	9750957	0	1060843	0	761723	0	0	0	0	0	0	0	0	0	0	0	25	0	0	0	25	0	36.45	0	6637949	0	0	0	-nan	18211472.0	16388906.0	0.0	9750957.0	1060843.0	761723.0	0.0	0.0	6637949.0	90.0	0.0	53.5	5.8	4.2	0.0	0.0	36.4
1458747	SRR1975423	SRP057202	SRS910982	SRX996685	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658719: WT_CSD2; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658719		GSM1658719	WT_CSD2	311784012	18340236	2016-04-14 16:08:07	254953382	311784012	18340236	1	18340236	index:0,count:18340236,average:17,stdev:0	GSM1658719_r1	GEO					2.6	4.78	0.11	283497648	230384263	120033668	117699155	81.26	98.06	0	0	0	0	0	0	37.42	88.7	40301612	6267177	40301612	6267177	58.74	84.91	40301612	9839073	40301612	5999431	51774561	18.26	0.00	0	52.80	0	5.21	0	3.46	0	0.00	0	0.00	0	16749736	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	504.01	0	0.00	0	0	0	18340236	0	9683753	0	956057	0	634443	0	0	0	0	0	0	0	0	0	0	0	27	0	0	0	27	0	38.53	0	7065983	0	0	0	-nan	18340236.0	16749736.0	0.0	9683753.0	956057.0	634443.0	0.0	0.0	7065983.0	91.3	0.0	52.8	5.2	3.5	0.0	0.0	38.5
1458762	SRR1975424	SRP057202	SRS910981	SRX996686	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658720: WT_CSD3; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658720		GSM1658720	WT_CSD3	309141872	18184816	2016-04-14 16:08:07	256034566	309141872	18184816	1	18184816	index:0,count:18184816,average:17,stdev:0	GSM1658720_r1	GEO					1.81	4.63	0.14	277576486	220701311	109998127	107913136	79.51	98.1	0	0	0	0	0	0	35.23	89.2	41509914	5775441	41509914	5775441	56.05	85.25	41509914	9189167	41509914	5519597	53416267	19.24	0.00	0	54.56	0	5.94	0	3.90	0	0.00	0	0.00	0	16395466	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	559.53	0	0.00	0	0	0	18184816	0	9921009	0	1080742	0	708608	0	0	0	0	0	0	0	0	0	0	0	28	0	0	0	28	0	35.60	0	6474457	0	0	0	-nan	18184816.0	16395466.0	0.0	9921009.0	1080742.0	708608.0	0.0	0.0	6474457.0	90.2	0.0	54.6	5.9	3.9	0.0	0.0	35.6
1458781	SRR1975425	SRP057202	SRS910979	SRX996687	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658721: WT_CSD4; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658721		GSM1658721	WT_CSD4	107757611	6338683	2016-04-14 16:08:07	92415202	107757611	6338683	1	6338683	index:0,count:6338683,average:17,stdev:0	GSM1658721_r1	GEO					2.04	4.96	0.13	95250771	74893473	38389852	36408177	78.63	94.84	0	0	0	0	0	0	33.16	82.95	14221383	1875783	14221383	1875783	54.01	79.52	14221383	3054701	14221383	1798328	19609856	20.59	0.00	0	53.56	0	4.83	0	5.94	0	0.00	0	0.00	0	5656216	0	17	0	16.98	0	0.00	0	0.00	0	0.00	0	0.00	0	518.62	0	0.00	0	0	0	6338683	0	3394816	0	306253	0	376214	0	0	0	0	0	0	0	0	0	0	0	5	0	0	0	5	0	35.68	0	2261400	0	0	0	-nan	6338683.0	5656216.0	0.0	3394816.0	306253.0	376214.0	0.0	0.0	2261400.0	89.2	0.0	53.6	4.8	5.9	0.0	0.0	35.7
1458795	SRR1975426	SRP057202	SRS910979	SRX996687	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658721: WT_CSD4; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658721		GSM1658721	WT_CSD4	444142798	20188309	2016-04-14 16:08:07	347530876	444142798	20188309	1	20188309	index:0,count:20188309,average:22,stdev:0	GSM1658721_r2	GEO					4.49	4.48	0.18	408361434	355831285	293370343	277393836	87.14	94.55	0	0	0	0	0	0	59.23	83.8	31696161	11514703	31696161	11514703	68.71	79.76	31696161	13356259	31696161	10959090	47253765	11.57	0.00	0	28.23	0	1.93	0	1.76	0	0.00	0	0.01	0	19439406	0	22	0	21.35	0	1.00	0	0.00	0	0.00	0	0.00	0	217.60	0	0.12	0	0	0	20188309	0	5699324	0	390204	0	355855	0	0	0	2844	0	0	0	0	0	102	0	31050	0	0	0	31152	0	68.06	0	13740082	0	0	0	-nan	20188309.0	19439406.0	0.0	5699324.0	390204.0	355855.0	0.0	2844.0	13740082.0	96.3	0.0	28.2	1.9	1.8	0.0	0.0	68.1
1458811	SRR1975427	SRP057202	SRS910978	SRX996688	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658722: WT_CSD5; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;induction of cortical spreading depression|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658722		GSM1658722	WT_CSD5	842187522	38281251	2016-04-14 16:08:07	636273457	842187522	38281251	1	38281251	index:0,count:38281251,average:22,stdev:0	GSM1658722_r1	GEO					3.52	4.44	0.13	770833032	677757238	556693744	534289287	87.93	95.98	0	0	0	0	0	0	60.46	85.28	60415287	22251321	60415287	22251321	68.99	81.14	60415287	25389500	60415287	21170661	91560303	11.88	0.00	0	27.99	0	1.89	0	1.95	0	0.00	0	0.02	0	36804288	0	22	0	21.34	0	1.00	0	0.00	0	1.00	0	0.00	0	206.00	0	0.14	0	0	0	38281251	0	10713386	0	725249	0	744768	0	0	0	6946	0	0	0	0	0	210	0	66882	0	0	0	67092	0	68.16	0	26090902	0	0	0	-nan	38281251.0	36804288.0	0.0	10713386.0	725249.0	744768.0	0.0	6946.0	26090902.0	96.1	0.0	28.0	1.9	1.9	0.0	0.0	68.2
1458841	SRR1975429	SRP057202	SRS910976	SRX996690	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658724: WT_SHAM1; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658724		GSM1658724	WT_SHAM1	189544084	11149652	2016-04-14 16:08:07	157975474	189544084	11149652	1	11149652	index:0,count:11149652,average:17,stdev:0	GSM1658724_r1	GEO					2.41	4.59	0.1	169340923	135341281	66846393	65518437	79.92	98.01	0	0	0	0	0	0	34.76	88.39	25191813	3477831	25191813	3477831	56.24	84.29	25191813	5627031	25191813	3316785	32854163	19.40	0.00	0	54.44	0	6.04	0	4.22	0	0.00	0	0.00	0	10005114	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	514.60	0	0.00	0	0	0	11149652	0	6070300	0	673979	0	470559	0	0	0	0	0	0	0	0	0	0	0	19	0	0	0	19	0	35.29	0	3934814	0	0	0	-nan	11149652.0	10005114.0	0.0	6070300.0	673979.0	470559.0	0.0	0.0	3934814.0	89.7	0.0	54.4	6.0	4.2	0.0	0.0	35.3
1458952	SRR1975430	SRP057202	SRS910975	SRX996691	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658725: WT_SHAM2; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658725		GSM1658725	WT_SHAM2	375137249	22066897	2016-04-14 16:08:07	310907018	375137249	22066897	1	22066897	index:0,count:22066897,average:17,stdev:0	GSM1658725_r1	GEO					2.65	4.52	0.1	337085720	270672038	134695693	132230575	80.3	98.17	0	0	0	0	0	0	35.44	89.0	49648345	7056173	49648345	7056173	57.16	85.0	49648345	11381104	49648345	6738845	63589630	18.86	0.00	0	54.31	0	5.86	0	3.90	0	0.00	0	0.00	0	19912621	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	645.86	0	0.00	0	0	0	22066897	0	11984290	0	1293338	0	860938	0	0	0	0	0	0	0	0	0	0	0	20	0	0	0	20	0	35.93	0	7928331	0	0	0	-nan	22066897.0	19912621.0	0.0	11984290.0	1293338.0	860938.0	0.0	0.0	7928331.0	90.2	0.0	54.3	5.9	3.9	0.0	0.0	35.9
1458968	SRR1975431	SRP057202	SRS910974	SRX996692	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658726: WT_SHAM3; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658726		GSM1658726	WT_SHAM3	266810971	15694763	2016-04-14 16:08:07	221521800	266810971	15694763	1	15694763	index:0,count:15694763,average:17,stdev:0	GSM1658726_r1	GEO					2.29	4.49	0.11	238724052	190926551	94570624	92837236	79.98	98.17	0	0	0	0	0	0	35.16	89.05	35494545	4956606	35494545	4956606	56.81	85.09	35494545	8009249	35494545	4736215	45269682	18.96	0.00	0	54.37	0	5.98	0	4.19	0	0.00	0	0.00	0	14098987	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	482.92	0	0.00	0	0	0	15694763	0	8532707	0	937963	0	657813	0	0	0	0	0	0	0	0	0	0	0	16	0	0	0	16	0	35.47	0	5566280	0	0	0	-nan	15694763.0	14098987.0	0.0	8532707.0	937963.0	657813.0	0.0	0.0	5566280.0	89.8	0.0	54.4	6.0	4.2	0.0	0.0	35.5
1458984	SRR1975432	SRP057202	SRS910973	SRX996693	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658727: WT_SHAM4; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658727		GSM1658727	WT_SHAM4	593796196	34929188	2016-04-14 16:08:07	478175262	593796196	34929188	1	34929188	index:0,count:34929188,average:17,stdev:0	GSM1658727_r1	GEO					2.44	4.51	0.09	532197407	425511082	213193039	210193297	79.95	98.59	0	0	0	0	0	0	35.83	89.72	78493573	11258045	78493573	11258045	56.91	85.63	78493573	17883088	78493573	10744516	100133967	18.82	0.00	0	54.04	0	5.91	0	4.13	0	0.00	0	0.00	0	31423318	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	595.95	0	0.00	0	0	0	34929188	0	18875854	0	2062743	0	1443127	0	0	0	0	0	0	0	0	0	0	0	21	0	0	0	21	0	35.92	0	12547464	0	0	0	-nan	34929188.0	31423318.0	0.0	18875854.0	2062743.0	1443127.0	0.0	0.0	12547464.0	90.0	0.0	54.0	5.9	4.1	0.0	0.0	35.9
1459000	SRR1975433	SRP057202	SRS910972	SRX996694	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658728: WT_SHAM5; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658728		GSM1658728	WT_SHAM5	478382788	28140164	2016-04-14 16:08:07	402369252	478382788	28140164	1	28140164	index:0,count:28140164,average:17,stdev:0	GSM1658728_r1	GEO					2.37	4.63	0.15	406358538	308343827	152584479	141633621	75.88	92.82	0	0	0	0	0	0	29.5	79.29	64264855	7129842	64264855	7129842	49.14	75.89	64264855	11877962	64264855	6824177	93646767	23.05	0.00	0	53.94	0	6.64	0	7.46	0	0.00	0	0.00	0	24169688	0	17	0	16.97	0	0.00	0	0.00	0	0.00	0	0.00	0	511.64	0	0.00	0	0	0	28140164	0	15177740	0	1869844	0	2100632	0	0	0	0	0	0	0	0	0	0	0	96	0	0	0	96	0	31.95	0	8991948	0	0	0	-nan	28140164.0	24169688.0	0.0	15177740.0	1869844.0	2100632.0	0.0	0.0	8991948.0	85.9	0.0	53.9	6.6	7.5	0.0	0.0	32.0
1459016	SRR1975434	SRP057202	SRS910971	SRX996695	SRA259335	GEO		RNA profiling by deepSAGE sequencing in the cortex of a migraine mouse model after induction of cortical spreading depression	Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Overall design: Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes		GSM1658729: WT_SHAM6; Mus musculus; RNA-Seq				RNA-Seq	TRANSCRIPTOMIC	cDNA	single			Frozen tissue of the mid-part of the cortex was crunched using a mortar and subsequently homogenized in lysis buffer using the Ultra-turrax T25 Polytron (Janke & Kunkel, Staufen, Germany) mechanical homogenizer. Total RNA was isolated using the Machery Nagel RNA isolation kit (Düren, Germany). Contaminating DNA was removed by on-column treatment with rDNase. Agilent 2100 Bioanalyzer total RNA nanochips (Agilent, Foster City, CA, USA) were used to determine RNA integrity. RNA samples included in this study had RIN (RNA integrity number) values between 8.9 and 10. mRNA was hybridized to Oligo(dT) beads. On the beads, double-stranded cDNA was synthesized, which was digested with Nlalll and Mmel restriction enzymes to create a 17-base-pair (bp) cDNA sequence. The sequence was flanked by two GEX adapters and amplified by PCR for 15 cycles, during which a 6-bp barcode index was introduced that allowed discrimination of reads from up to 12 different samples after sequencing.	Illumina HiSeq 2000	age;;2-4 months|genotype/variation;;wild-type|protocol;;sham surgery|source_name;;Middle cortex|strain;;C57BL/6J|tissue;;Middle cortex	GEO Accession;;GSM1658729		GSM1658729	WT_SHAM6	479468544	28204032	2016-04-14 16:08:07	387662333	479468544	28204032	1	28204032	index:0,count:28204032,average:17,stdev:0	GSM1658729_r1	GEO					3.38	4.54	0.13	429168372	345942447	172674576	169407997	80.61	98.11	0	0	0	0	0	0	35.63	88.85	62607718	9029950	62607718	9029950	57.94	85.12	62607718	14683909	62607718	8651144	80218892	18.69	0.00	0	53.82	0	5.91	0	4.23	0	0.00	0	0.00	0	25343368	0	17	0	16.99	0	0.00	0	0.00	0	0.00	0	0.00	0	576.90	0	0.00	0	0	0	28204032	0	15179890	0	1667860	0	1192804	0	0	0	0	0	0	0	0	0	0	0	58	0	0	0	58	0	36.04	0	10163478	0	0	0	-nan	28204032.0	25343368.0	0.0	15179890.0	1667860.0	1192804.0	0.0	0.0	10163478.0	89.9	0.0	53.8	5.9	4.2	0.0	0.0	36.0
1901594	SRR3167041	SRP064669	SRS1110082	SRX1583870	SRA353260	NCBI	IEB	Mus musculus domesticus Raw sequence reads	Test SRA submission		goosy cooked 1	goosy cooked at 350 C		goosy 1	RNA-Seq	TRANSCRIPTOMIC	RANDOM	paired				Illumina HiSeq 2500	age;;not collected|BioSampleModel;;Model organism or animal|birth_location;;Portoviejo|breeding_history;;Abdominal|collected_by;;Felipe de Mello Martins|collection_date;;27-Nov-2012|death_date;;28-Nov-12|geo_loc_name;;Ecuador: Portoviejo|lat_lon;;1.079383333 S 80.53991667 W|sex;;male|strain;;not collected|sub_species;;domesticus|tissue;;liver			FMM_48		612	6	2018-06-20 00:16:46	54300	612	6	2	6	index:0,count:6,average:51,stdev:0|index:1,count:6,average:51,stdev:0	A_R2.zip						0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0.00	0	0.00	0	0.00	0	0.00	0	0.00	0	100.00	0	0	0	102	0	0.00	0	0.00	0	0.00	0	0.00	0	0.00	0	0.01	0	0	0	0	0	6	0	0	0	0	0	0	0	0	0	6	0	0	0	0	0	0	0	0	0	0	0	0	0	0.00	0	0	0	0	0	-nan	6.0	0.0	0.0	0.0	0.0	0.0	0.0	6.0	0.0	0.0	0.0	0.0	0.0	0.0	0.0	100.0	0.0
1921311	SRR3180511	SRP064669	SRS1110082	SRX1594707	SRA355915	NIH		Mus musculus domesticus Raw sequence reads	Test SRA submission		goosy cooked 1	goosy cooked at 350 C		goosy 1	RNA-Seq	TRANSCRIPTOMIC	RANDOM	paired				Illumina HiSeq 2500	age;;not collected|BioSampleModel;;Model organism or animal|birth_location;;Portoviejo|breeding_history;;Abdominal|collected_by;;Felipe de Mello Martins|collection_date;;27-Nov-2012|death_date;;28-Nov-12|geo_loc_name;;Ecuador: Portoviejo|lat_lon;;1.079383333 S 80.53991667 W|sex;;male|strain;;not collected|sub_species;;domesticus|tissue;;liver			FMM_48		612	6	2018-06-20 00:16:46	54300	612	6	2	6	index:0,count:6,average:51,stdev:0|index:1,count:6,average:51,stdev:0	A_R1.zip						0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0.00	0	0.00	0	0.00	0	0.00	0	0.00	0	100.00	0	0	0	102	0	0.00	0	0.00	0	0.00	0	0.00	0	0.00	0	0.02	0	0	0	0	0	6	0	0	0	0	0	0	0	0	0	6	0	0	0	0	0	0	0	0	0	0	0	0	0	0.00	0	0	0	0	0	-nan	6.0	0.0	0.0	0.0	0.0	0.0	0.0	6.0	0.0	0.0	0.0	0.0	0.0	0.0	0.0	100.0	0.0
1921327	SRR3180512	SRP064669	SRS1110082	SRX1594708	SRA355915	NIH		Mus musculus domesticus Raw sequence reads	Test SRA submission		goosy cooked 1	goosy cooked at 350 C		goosy 2	RNA-Seq	TRANSCRIPTOMIC	RANDOM	paired				Illumina HiSeq 2500	age;;not collected|BioSampleModel;;Model organism or animal|birth_location;;Portoviejo|breeding_history;;Abdominal|collected_by;;Felipe de Mello Martins|collection_date;;27-Nov-2012|death_date;;28-Nov-12|geo_loc_name;;Ecuador: Portoviejo|lat_lon;;1.079383333 S 80.53991667 W|sex;;male|strain;;not collected|sub_species;;domesticus|tissue;;liver			FMM_48		612	6	2016-02-24 16:25:24	80734	612	6	2	6	index:0,count:6,average:51,stdev:0|index:1,count:6,average:51,stdev:0	A_R2.fastq.tar						0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0.00	0	0.00	0	0.00	0	0.00	0	0.00	0	100.00	0	0	0	102	0	0.00	0	0.00	0	0.00	0	0.00	0	0.00	0	0.02	0	0	0	0	0	6	0	0	0	0	0	0	0	0	0	6	0	0	0	0	0	0	0	0	0	0	0	0	0	0.00	0	0	0	0	0	-nan	6.0	0.0	0.0	0.0	0.0	0.0	0.0	6.0	0.0	0.0	0.0	0.0	0.0	0.0	0.0	100.0	0.0
1922906	SRR3090575	SRP064669	SRS1110082	SRX1521170	SRA331876	NCBI	IEB	Mus musculus domesticus Raw sequence reads	Test SRA submission		goosy cooked 7	goose cooked at 650 C		goosy 7	RNA-Seq	TRANSCRIPTOMIC	PCR	paired				Illumina HiSeq 2500	age;;not collected|BioSampleModel;;Model organism or animal|birth_location;;Portoviejo|breeding_history;;Abdominal|collected_by;;Felipe de Mello Martins|collection_date;;27-Nov-2012|death_date;;28-Nov-12|geo_loc_name;;Ecuador: Portoviejo|lat_lon;;1.079383333 S 80.53991667 W|sex;;male|strain;;not collected|sub_species;;domesticus|tissue;;liver			FMM_48		612	6	2016-01-12 11:49:18	80734	612	6	2	6	index:0,count:6,average:51,stdev:0|index:1,count:6,average:51,stdev:0	A_R2.fastq						0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0.00	0	0.00	0	0.00	0	0.00	0	0.00	0	100.00	0	0	0	102	0	0.00	0	0.00	0	0.00	0	0.00	0	0.00	0	0.02	0	0	0	0	0	6	0	0	0	0	0	0	0	0	0	6	0	0	0	0	0	0	0	0	0	0	0	0	0	0.00	0	0	0	0	0	-nan	6.0	0.0	0.0	0.0	0.0	0.0	0.0	6.0	0.0	0.0	0.0	0.0	0.0	0.0	0.0	100.0	0.0