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Elevated intraocular pressure (IOP) is a cause of glaucoma. However, glaucoma often develops with normal IOP and is known as normal\u2010tension glaucoma (NTG). Glutamate neurotoxicity is considered as one of the significant causes of NTG, resulting in excessive stimulation of retinal neurons via the N\u2010methyl\u2010D\u2010aspartate (NMDA) receptors. The present study examined the phosphorylation of collapsin response mediator protein\u20102 (CRMP2), a protein that is abundantly expressed in neurons and involved in their development. In two mouse models, NMDA\u2010injection and glutamate\/aspartate transporter (GLAST) mutant, CRMP2 phosphorylation at the cyclin\u2010dependent kinase\u20105 (Cdk5) site was elevated in RGCs. We confirmed that the decrease in the number of RGCs and thickness of the inner retinal layer (IRL) could be suppressed after NMDA administration in CRMP2KI\/KI mice with genetically inhibited CRMP2 phosphorylation. Next, we investigated GLAST heterozygotes (GLAST+\/\u2212) with CRMP2KI\/KI (GLAST+\/\u2212;CRMP2KI\/KI) and GLAST knockout (GLAST\u2212\/\u2212) mice with CRMP2KI\/KI (GLAST\u2212\/\u2212;CRMP2KI\/KI) mice and compared them with GLAST+\/\u2212 and GLAST\u2212\/\u2212 mice. pCRMP2 (S522) inhibition significantly reduced RGC loss and IRL thinning. These results suggest that the inhibition of CRMP2 phosphorylation could be a novel strategy for treating NTG.<\/jats:p>","DOI":"10.1111\/gtc.12971","type":"journal-article","created":{"date-parts":[[2022,6,15]],"date-time":"2022-06-15T09:14:07Z","timestamp":1655284447000},"page":"526-536","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Genetic inhibition of collapsin response mediator protein\u20102 phosphorylation ameliorates retinal ganglion cell death in normal\u2010tension glaucoma models"],"prefix":"10.1111","volume":"27","author":[{"given":"Musukha Mala","family":"Brahma","sequence":"first","affiliation":[{"name":"Department of Life Science and Medical Bio\u2010Science Waseda University  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuya","family":"Takahashi","sequence":"additional","affiliation":[{"name":"Department of Life Science and Medical Bio\u2010Science Waseda University  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuhiko","family":"Namekata","sequence":"additional","affiliation":[{"name":"Visual Research Project Tokyo Metropolitan Institute of Medical Science  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takayuki","family":"Harada","sequence":"additional","affiliation":[{"name":"Visual Research Project Tokyo Metropolitan Institute of Medical Science  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshio","family":"Goshima","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Neurobiology Yokohama City University Graduate School of Medicine  Yokohama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4931-7087","authenticated-orcid":false,"given":"Toshio","family":"Ohshima","sequence":"additional","affiliation":[{"name":"Department of Life Science and Medical 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