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The Function of the NMDA Receptor in Hypoxic-Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is one of the main forms of neonatal brain injury which could lead to neonatal disability or even cause neonatal death. Therefore, HIE strongly affects the health of newborns and brings heavy burden to the family and society. It has been well studied that N-meth...

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Detalles Bibliográficos
Autores principales: Zhang, Xiaotong, Peng, Kaizhen, Zhang, Xiaomin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573650/
https://www.ncbi.nlm.nih.gov/pubmed/33117117
http://dx.doi.org/10.3389/fnins.2020.567665
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author Zhang, Xiaotong
Peng, Kaizhen
Zhang, Xiaomin
author_facet Zhang, Xiaotong
Peng, Kaizhen
Zhang, Xiaomin
author_sort Zhang, Xiaotong
collection PubMed
description Hypoxic-ischemic encephalopathy (HIE) is one of the main forms of neonatal brain injury which could lead to neonatal disability or even cause neonatal death. Therefore, HIE strongly affects the health of newborns and brings heavy burden to the family and society. It has been well studied that N-methyl-D-aspartate (NMDA) receptors are involved in the excitotoxicity induced by hypoxia ischemia in adult brain. Recently, it has been shown that the NMDA receptor also plays important roles in HIE. In the present review, we made a summary of the molecular mechanism of NMDA receptor in the pathological process of HIE, focusing on the distinct role of GluN2A- and GluN2B-containing NMDA receptor subtypes and aiming to provide some insights into the clinical treatment and drug development of HIE.
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spelling pubmed-75736502020-10-27 The Function of the NMDA Receptor in Hypoxic-Ischemic Encephalopathy Zhang, Xiaotong Peng, Kaizhen Zhang, Xiaomin Front Neurosci Neuroscience Hypoxic-ischemic encephalopathy (HIE) is one of the main forms of neonatal brain injury which could lead to neonatal disability or even cause neonatal death. Therefore, HIE strongly affects the health of newborns and brings heavy burden to the family and society. It has been well studied that N-methyl-D-aspartate (NMDA) receptors are involved in the excitotoxicity induced by hypoxia ischemia in adult brain. Recently, it has been shown that the NMDA receptor also plays important roles in HIE. In the present review, we made a summary of the molecular mechanism of NMDA receptor in the pathological process of HIE, focusing on the distinct role of GluN2A- and GluN2B-containing NMDA receptor subtypes and aiming to provide some insights into the clinical treatment and drug development of HIE. Frontiers Media S.A. 2020-10-06 /pmc/articles/PMC7573650/ /pubmed/33117117 http://dx.doi.org/10.3389/fnins.2020.567665 Text en Copyright © 2020 Zhang, Peng and Zhang. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Zhang, Xiaotong
Peng, Kaizhen
Zhang, Xiaomin
The Function of the NMDA Receptor in Hypoxic-Ischemic Encephalopathy
title The Function of the NMDA Receptor in Hypoxic-Ischemic Encephalopathy
title_full The Function of the NMDA Receptor in Hypoxic-Ischemic Encephalopathy
title_fullStr The Function of the NMDA Receptor in Hypoxic-Ischemic Encephalopathy
title_full_unstemmed The Function of the NMDA Receptor in Hypoxic-Ischemic Encephalopathy
title_short The Function of the NMDA Receptor in Hypoxic-Ischemic Encephalopathy
title_sort function of the nmda receptor in hypoxic-ischemic encephalopathy
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573650/
https://www.ncbi.nlm.nih.gov/pubmed/33117117
http://dx.doi.org/10.3389/fnins.2020.567665
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