Sustained Hypoxia Alters nTS Glutamatergic Signaling and Expression and Function of Excitatory Amino Acid Transporters.
astroglia
autonomic nervous system
chemoreflex
glutamate
respiration
synaptic transmission
Journal
Neuroscience
ISSN: 1873-7544
Titre abrégé: Neuroscience
Pays: United States
ID NLM: 7605074
Informations de publication
Date de publication:
15 03 2020
15 03 2020
Historique:
received:
05
10
2019
revised:
11
01
2020
accepted:
23
01
2020
pubmed:
8
2
2020
medline:
15
5
2021
entrez:
8
2
2020
Statut:
ppublish
Résumé
Glutamate is the major excitatory neurotransmitter in the nucleus tractus solitarii (nTS) and mediates chemoreflex function during periods of low oxygen (i.e. hypoxia). We have previously shown that nTS excitatory amino acid transporters (EAATs), specifically EAAT-2, located on glia modulate neuronal activity, cardiorespiratory and chemoreflex function under normal conditions via its tonic uptake of extracellular glutamate. Chronic sustained hypoxia (SH) elevates nTS synaptic transmission and chemoreflex function. The goal of this study was to determine the extent to which glial EAAT-2 contributes to SH-induced nTS synaptic alterations. To do so, male Sprague-Dawley rats (4-7 weeks) were exposed to either 1, 3, or 7 days of SH (10% O
Identifiants
pubmed: 32032667
pii: S0306-4522(20)30057-9
doi: 10.1016/j.neuroscience.2020.01.034
pmc: PMC7560968
mid: NIHMS1556805
pii:
doi:
Substances chimiques
Amino Acid Transport Systems
0
Neurotransmitter Agents
0
Glutamic Acid
3KX376GY7L
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
131-140Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL055306
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128454
Pays : United States
Informations de copyright
Copyright © 2020 IBRO. Published by Elsevier Ltd. All rights reserved.
Références
J Neurophysiol. 2002 Nov;88(5):2736-44
pubmed: 12424308
J Neurophysiol. 2017 Apr 1;117(4):1625-1635
pubmed: 28100653
J Neurosci. 2007 Apr 25;27(17):4663-73
pubmed: 17460079
J Physiol. 2014 Apr 15;592(8):1839-56
pubmed: 24492841
Am J Physiol Lung Cell Mol Physiol. 2002 Jun;282(6):L1314-23
pubmed: 12003788
Front Mol Neurosci. 2019 Jul 09;12:164
pubmed: 31338020
Brain Res. 2016 Mar 15;1635:12-26
pubmed: 26779891
Respir Physiol Neurobiol. 2008 Dec 10;164(1-2):105-11
pubmed: 18524694
J Neurosci. 2007 Apr 11;27(15):3946-55
pubmed: 17428968
PLoS One. 2013 Aug 12;8(8):e70791
pubmed: 23951010
J Physiol. 2001 Feb 15;531(Pt 1):165-70
pubmed: 11179400
Annu Rev Physiol. 1994;56:93-116
pubmed: 7912060
Respir Physiol. 2000 Jul;121(2-3):223-36
pubmed: 10963777
Neuroscience. 2010 May 5;167(2):510-27
pubmed: 20153814
J Physiol. 2017 Sep 1;595(17):6045-6063
pubmed: 28677303
Respir Physiol Neurobiol. 2005 Apr 15;146(2-3):269-77
pubmed: 15766915
Respir Physiol Neurobiol. 2009 Sep 30;168(3):272-80
pubmed: 19619674
Am J Physiol. 1992 Aug;263(2 Pt 2):R368-75
pubmed: 1510176
Front Physiol. 2018 Feb 27;9:134
pubmed: 29535636
J Neurosci. 2015 Apr 29;35(17):6903-17
pubmed: 25926465
J Neurophysiol. 2019 May 1;121(5):1822-1830
pubmed: 30892977
J Neurosci Res. 2014 May;92(5):627-33
pubmed: 24510616
J Neurosci. 2005 Mar 30;25(13):3389-99
pubmed: 15800194
J Physiol. 1994 Jul 1;478 ( Pt 1):55-66
pubmed: 7965835
J Neurophysiol. 2012 Oct;108(8):2292-305
pubmed: 22855775
J Neurosci. 2009 Mar 11;29(10):3093-102
pubmed: 19279246
Brain Res. 1992 Feb 14;572(1-2):108-16
pubmed: 1611506
Am J Physiol. 1999 Oct;277(4):H1350-60
pubmed: 10516169
J Physiol. 1993 Sep;469:341-63
pubmed: 7505824
Methods. 2001 Dec;25(4):402-8
pubmed: 11846609
J Physiol. 2019 Jun;597(11):2903-2923
pubmed: 30993693
J Appl Physiol (1985). 1999 Aug;87(2):817-23
pubmed: 10444644
Glia. 2011 Apr;59(4):655-63
pubmed: 21294164
J Neurophysiol. 2016 Mar;115(3):1691-702
pubmed: 26719090
J Neurophysiol. 2001 May;85(5):2213-23
pubmed: 11353036