TRPV1 channels contribute to spontaneous glutamate release in nucleus tractus solitarii following chronic intermittent hypoxia.
autonomic nervous system
calcium channels
intermittent hypoxia
respiration
synaptic transmission
Journal
Journal of neurophysiology
ISSN: 1522-1598
Titre abrégé: J Neurophysiol
Pays: United States
ID NLM: 0375404
Informations de publication
Date de publication:
01 03 2019
01 03 2019
Historique:
pubmed:
3
1
2019
medline:
26
2
2020
entrez:
3
1
2019
Statut:
ppublish
Résumé
Chronic intermittent hypoxia (CIH) reduces afferent-evoked excitatory postsynaptic currents (EPSCs) but enhances basal spontaneous (s) and asynchronous (a) EPSCs in second-order neurons of nucleus tractus solitarii (nTS), a major area for cardiorespiratory control. The net result is an increase in synaptic transmission. The mechanisms by which this occurs are unknown. The N-type calcium channel and transient receptor potential cation channel TRPV1 play prominent roles in nTS sEPSCs and aEPSCs. The functional role of these channels in CIH-mediated afferent-evoked EPSC, sEPSC, and aEPSC was tested in rat nTS slices following antagonist inhibition and in mouse nTS slices that lack TRPV1. Block of N-type channels decreased aEPSCs in normoxic and, to a lesser extent, CIH-exposed rats. sEPSCs examined in the presence of TTX (miniature EPSCs) were also decreased by N-type block in normoxic but not CIH-exposed rats. Antagonist inhibition of TRPV1 reduced the normoxic and the CIH-mediated increase in sEPSCs, aEPSCs, and mEPSCs. As in rats, in TRPV1
Identifiants
pubmed: 30601692
doi: 10.1152/jn.00536.2018
pmc: PMC6520621
doi:
Substances chimiques
TRPV Cation Channels
0
TRPV1 protein, mouse
0
Glutamic Acid
3KX376GY7L
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
881-892Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL128454
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL090886
Pays : United States
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