<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE237nnn/GSE237027/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE237027</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptomic changes in Grin2b-C456Y-mutant mice with NMDAR activation</name><description>Our previous study reported a Grin2b-mutant mouse line carrying a point mutation identified in individuals with ASD (Grin2b+/C456Y mice), which show suppressed long-term depression and anxiolytic-like behavior that are responsive to early chronic D-cycloserine (DCS) treatment (postnatal day 7 to 16) for pharmacological activation of NMDARs. To figure out the rescue mechanism, we attempted RNA-Seq analysis of wild-type (WT) and Grin2b+/C456Y mice that are early and chronically treated with vehicle and DCS.</description><dates><publication>2026/07/09</publication></dates><accession>GSE237027</accession><cross_references><GSM>GSM7593209</GSM><GSM>GSM7593219</GSM><GSM>GSM7593208</GSM><GSM>GSM7593218</GSM><GSM>GSM7593207</GSM><GSM>GSM7593213</GSM><GSM>GSM7593202</GSM><GSM>GSM7593212</GSM><GSM>GSM7593201</GSM><GSM>GSM7593211</GSM><GSM>GSM7593200</GSM><GSM>GSM7593210</GSM><GSM>GSM7593199</GSM><GSM>GSM7593217</GSM><GSM>GSM7593206</GSM><GSM>GSM7593216</GSM><GSM>GSM7593205</GSM><GSM>GSM7593215</GSM><GSM>GSM7593204</GSM><GSM>GSM7593214</GSM><GSM>GSM7593203</GSM><GSM>GSM7593198</GSM><GSM>GSM7593197</GSM><GPL>24247</GPL><GSE>237027</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>