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Glutamate excitotoxicity is thought to play a critical role in many CNS and retinal diseases. Accordingly, glutamate excitotoxicity has been used as a model to study neuronal diseases. Immune proteins, such as major histocompatibility complex (MHC) class I molecules and their receptors, play important roles in many neuronal diseases, while T-cell receptors (TCR) are the primary receptors of MHCI. We previously showed that a critical component of TCR, CD3\u03b6, is expressed by mouse retinal ganglion cells (RGCs). The mutation of CD3\u03b6 or MHCI molecules compromises the development of RGC structure and function. In this study, we investigated whether CD3\u03b6-mediated molecular signaling regulates RGC death in glutamate excitotoxicity. We show that mutation of CD3\u03b6 significantly increased RGC survival in NMDA-induced excitotoxicity. In addition, we found that several downstream molecules of TCR, including Src (proto-oncogene tyrosine-protein kinase) family kinases (SFKs) and spleen tyrosine kinase (Syk), are expressed by RGCs. Selective inhibition of an SFK member, Hck, or Syk members, Syk or Zap70, significantly increased RGC survival in NMDA-induced excitotoxicity. These results provide direct evidence to reveal the underlying molecular mechanisms that control RGC death under disease conditions.<\/jats:p>","DOI":"10.3390\/cells13121006","type":"journal-article","created":{"date-parts":[[2024,6,10]],"date-time":"2024-06-10T08:49:03Z","timestamp":1718009343000},"page":"1006","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["CD3\u03b6-Mediated Signaling Protects Retinal Ganglion Cells in Glutamate Excitotoxicity of the Retina"],"prefix":"10.3390","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-9753-4392","authenticated-orcid":false,"given":"Rui","family":"Du","sequence":"first","affiliation":[{"name":"Department of Ophthalmology and Visual Science, University of Utah School of Medicine, Salt Lake City, UT 84132, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ping","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Visual Science, University of Utah School of Medicine, Salt Lake City, UT 84132, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0491-278X","authenticated-orcid":false,"given":"Ning","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Visual Science, University of Utah School of Medicine, Salt Lake City, UT 84132, USA"},{"name":"Department of Neurobiology, University of Utah, Salt Lake City, UT 84132, USA"},{"name":"Department of Biomedical Engineering, University of Utah, Salt Lake City, UT 84132, USA"},{"name":"Veterans Affairs Medical Center, Salt Lake City, UT 84148, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,6,8]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"383","DOI":"10.1016\/j.ohc.2005.04.002","article-title":"Retinal Ganglion Cell Death in Glaucoma: Mechanisms and Neuroprotective Strategies","volume":"18","author":"Kuehn","year":"2005","journal-title":"Ophthalmol. 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