<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Andrews WT</submitter><funding>NIA NIH HHS</funding><funding>National Institute of General Medical Sciences</funding><funding>NIH HHS</funding><funding>National Institute on Aging</funding><funding>NIGMS NIH HHS</funding><pagination>6275-6285</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7483268</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>412(24)</volume><pubmed_abstract>The N-methyl-D-aspartate (NMDA) receptor is a crucial mediator of pathological glutamate-driven excitotoxicity and subsequent neuronal death in acute ischemic stroke. Although the roles of the NMDAR's composite GluN2A-C subunits have been investigated in this phenomenon, the relative importance of the GluN2D subunit has yet to be evaluated. Herein, GluN2D&lt;sup>-/-&lt;/sup> mice were studied in a model of ischemic stroke using MALDI FT-ICR mass spectrometry imaging to investigate the role of the GluN2D subunit of the NMDA receptor in brain ischemia. GluN2D&lt;sup>-/-&lt;/sup> mice underwent middle cerebral artery occlusion (MCAO) and brain tissue was subsequently harvested, frozen, and cryosectioned. Tissue sections were analyzed via MALDI FT-ICR mass spectrometry imaging. MALDI analyses revealed inc</pubmed_abstract><journal>Analytical and bioanalytical chemistry</journal><pubmed_title>In situ metabolite and lipid analysis of GluN2D&lt;sup>-/-&lt;/sup> and wild-type mice after ischemic stroke using MALDI MSI.</pubmed_title><pmcid>PMC7483268</pmcid><funding_grant_id>R21-AG062144</funding_grant_id><funding_grant_id>S10 OD018507</funding_grant_id><funding_grant_id>R01 GM110406</funding_grant_id><funding_grant_id>R21 AG062144</funding_grant_id><pubmed_authors>Andrews WT</pubmed_authors><pubmed_authors>Holmes A</pubmed_authors><pubmed_authors>Castellino FJ</pubmed_authors><pubmed_authors>Hummon AB</pubmed_authors><pubmed_authors>Donahue D</pubmed_authors><pubmed_authors>Balsara R</pubmed_authors></additional><is_claimable>false</is_claimable><name>In situ metabolite and lipid analysis of GluN2D&lt;sup>-/-&lt;/sup> and wild-type mice after ischemic stroke using MALDI MSI.</name><description>The N-methyl-D-aspartate (NMDA) receptor is a crucial mediator of pathological glutamate-driven excitotoxicity and subsequent neuronal death in acute ischemic stroke. Although the roles of the NMDAR's composite GluN2A-C subunits have been investigated in this phenomenon, the relative importance of the GluN2D subunit has yet to be evaluated. Herein, GluN2D&lt;sup>-/-&lt;/sup> mice were studied in a model of ischemic stroke using MALDI FT-ICR mass spectrometry imaging to investigate the role of the GluN2D subunit of the NMDA receptor in brain ischemia. GluN2D&lt;sup>-/-&lt;/sup> mice underwent middle cerebral artery occlusion (MCAO) and brain tissue was subsequently harvested, frozen, and cryosectioned. Tissue sections were analyzed via MALDI FT-ICR mass spectrometry imaging. MALDI analyses revealed inc</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Sep</publication><modification>2025-04-04T00:38:25.944Z</modification><creation>2022-02-11T10:02:18.648Z</creation></dates><accession>S-EPMC7483268</accession><cross_references><pubmed>32107573</pubmed><doi>10.1007/s00216-020-02477-z</doi></cross_references></HashMap>