Retinal glutamate neurotransmission

• Verfasst von: Boccuni, Isabella [VerfasserIn]
• Verfasst von: Fairless, Richard [VerfasserIn]
• Titel: Retinal glutamate neurotransmission
• Titelzusatz: from physiology to pathophysiological mechanisms of retinal ganglion cell degeneration
• Verf.angabe: Isabella Boccuni and Richard Fairless
• E-Jahr: 2022
• Jahr: 25 April 2022
• Umfang: 33 S.
• Fussnoten: Gesehen am 07.07.2022 ; This article belongs to the special issue "New insights on cellular biology of retinal degenerations"
• Titel Quelle: Enthalten in: Life
• Ort Quelle: Basel : MDPI, 2011
• Jahr Quelle: 2022
• Band/Heft Quelle: 12(2022), 5, special issue, Artikel-ID 638, Seite 1-33
• ISSN Quelle: 2075-1729
• DOI: doi:10.3390/life12050638
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: excitotoxicity
• Sach-SW: glutamate
• Sach-SW: neuronal vulnerability
• Sach-SW: NMDA receptor
• Sach-SW: retina
• Sach-SW: retinal ganglion cell
• K10plus-PPN: 1809445582

Abstract

Glutamate neurotransmission and metabolism are finely modulated by the retinal network, where the efficient processing of visual information is shaped by the differential distribution and composition of glutamate receptors and transporters. However, disturbances in glutamate homeostasis can result in glutamate excitotoxicity, a major initiating factor of common neurodegenerative diseases. Within the retina, glutamate excitotoxicity can impair visual transmission by initiating degeneration of neuronal populations, including retinal ganglion cells (RGCs). The vulnerability of RGCs is observed not just as a result of retinal diseases but has also been ascribed to other common neurodegenerative and peripheral diseases. In this review, we describe the vulnerability of RGCs to glutamate excitotoxicity and the contribution of different glutamate receptors and transporters to this. In particular, we focus on the N-methyl-d-aspartate (NMDA) receptor as the major effector of glutamate-induced mechanisms of neurodegeneration, including impairment of calcium homeostasis, changes in gene expression and signalling, and mitochondrial dysfunction, as well as the role of endoplasmic reticular stress. Due to recent developments in the search for modulators of NMDA receptor signalling, novel neuroprotective strategies may be on the horizon.