Visual Disfunction due to the Selective Effect of Glutamate Agonists on Retinal Cells

Autor: Nicolás Cuenca, Ariadna Díaz-Tahoces, Eduardo Fernández, Pedro de la Villa, Santiago Milla-Navarro, Isabel Ortuño-Lizarán, Francisco Germain
Přispěvatelé: Universidad de Alicante. Departamento de Fisiología, Genética y Microbiología, Neurobiología del Sistema Visual y Terapia de Enfermedades Neurodegenerativas (NEUROVIS)
Rok vydání: 2021
Předmět:
Retinal Ganglion Cells
Excitotoxicity
Apoptosis
medicine.disease_cause
Amacrine cell
chemistry.chemical_compound
Mice
0302 clinical medicine
excitoxicity
pERG
Excitatory Amino Acid Agonists
Retinal ganglion cell
Biology (General)
retinal ganglion cell
Bipolar cell
Spectroscopy
General Medicine
Computer Science Applications
bipolar cell
Chemistry
medicine.anatomical_structure
Receptors
Glutamate
NMDA receptor
Kainic acid
N-Methylaspartate
QH301-705.5
optomotor test
Vision Disorders
Glutamic Acid
Biología Celular
Retinal ganglion
Receptors
N-Methyl-D-Aspartate
Article
Catalysis
Inorganic Chemistry
03 medical and health sciences
Multielectrode recording
medicine
Animals
Physical and Theoretical Chemistry
QD1-999
Molecular Biology
Retina
kinate
multielectrode recording
Organic Chemistry
Kinate
Retinal
Excitoxicity
Optomotor test
Mice
Inbred C57BL
Amacrine Cells
chemistry
NMDA
030221 ophthalmology & optometry
sense organs
Neuroscience
030217 neurology & neurosurgery
amacrine cell
Zdroj: RUA. Repositorio Institucional de la Universidad de Alicante
Universidad de Alicante (UA)
International Journal of Molecular Sciences
Volume 22
Issue 12
International Journal of Molecular Sciences, Vol 22, Iss 6245, p 6245 (2021)
ISSN: 1422-0067
Popis: One of the causes of nervous system degeneration is an excess of glutamate released upon several diseases. Glutamate analogs, like N-methyl-DL-aspartate (NMDA) and kainic acid (KA), have been shown to induce experimental retinal neurotoxicity. Previous results have shown that NMDA/KA neurotoxicity induces significant changes in the full field electroretinogram response, a thinning on the inner retinal layers, and retinal ganglion cell death. However, not all types of retinal neurons experience the same degree of injury in response to the excitotoxic stimulus. The goal of the present work is to address the effect of intraocular injection of different doses of NMDA/KA on the structure and function of several types of retinal cells and their functionality. To globally analyze the effect of glutamate receptor activation in the retina after the intraocular injection of excitotoxic agents, a combination of histological, electrophysiological, and functional tools has been employed to assess the changes in the retinal structure and function. Retinal excitotoxicity caused by the intraocular injection of a mixture of NMDA/KA causes a harmful effect characterized by a great loss of bipolar, amacrine, and retinal ganglion cells, as well as the degeneration of the inner retina. This process leads to a loss of retinal cell functionality characterized by an impairment of light sensitivity and visual acuity, with a strong effect on the retinal OFF pathway. The structural and functional injury suffered by the retina suggests the importance of the glutamate receptors expressed by different types of retinal cells. The effect of glutamate agonists on the OFF pathway represents one of the main findings of the study, as the evaluation of the retinal lesions caused by excitotoxicity could be specifically explored using tests that evaluate the OFF pathway. This study was funded by the Instituto de Salud Carlos III (RETICS-FEDER RD16/0008/0016, RD16/0008/0020, and FIS/PI18-00754) and cofounded with the European Regional Development Fund (ERDF) within the “Plan Estatal de Investigación Científica y Técnica y de Innovación 2017–2020”, the Spanish Ministry of Economy and Competitiveness (RTI2018-098969-B-100 and FEDER-PID2019-106230-RB-100), Generalitat Valenciana (PROMETEO/2017/060, IDIFEDER/2017/064, and APOSTD/2020/245), and by the Bidons Egara Research Chair of the University Miguel Hernández.
Databáze: OpenAIRE
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