Loss of excitatory amino acid transporter restraint following chronic intermittent hypoxia contributes to synaptic alterations in nucleus tractus solitarii-Reference-Cited by-同舟云学术

Loss of excitatory amino acid transporter restraint following chronic intermittent hypoxia contributes to synaptic alterations in nucleus tractus solitarii

Published:2020-06-01 Issue:6 Volume:123 Page:2122-2135
ISSN:0022-3077
Container-title:Journal of Neurophysiology
language:en
Short-container-title:Journal of Neurophysiology

Author:

Martinez Diana¹^ORCID,Rogers Richard C.²^ORCID,Hasser Eileen M.¹³^ORCID,Hermann Gerlinda E.²^ORCID,Kline David D.¹^ORCID

Affiliation:

1. Department of Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri

2. Pennington Biomedical Research Center, Baton Rouge, Louisiana

3. Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, Missouri

Abstract

Removal of excitatory amino acid transporter (EAAT) restraint increases spontaneous synaptic activity yet decreases afferent [tractus solitarii (TS)]-driven excitatory postsynaptic current (EPSC) amplitude. In the chronic intermittent hypoxia model of obstructive sleep apnea, this restraint is lost due to reduction in EAAT expression and function. Thus EAATs are important in controlling elevated glutamatergic signaling, and loss of such control results in maladaptive synaptic signaling.

Funder

HHS | NIH | National Heart, Lung, and Blood Institute

American Heart Association

HHS | National Institutes of Health

Publisher

American Physiological Society

Subject

Physiology,General Neuroscience

Link

https://journals.physiology.org/doi/pdf/10.1152/jn.00766.2019

Reference75 articles.

1. Obstructive sleep apnea and insight into mechanisms of sympathetic overactivity