Glutamate potentiates heterologously expressed homomeric acid-sensing ion channel 1a.
acid-sensing ion channel (ASIC)
drug action
glutamate
ligand-gated ion channel
pharmacology
Journal
Synapse (New York, N.Y.)
ISSN: 1098-2396
Titre abrégé: Synapse
Pays: United States
ID NLM: 8806914
Informations de publication
Date de publication:
04 2022
04 2022
Historique:
revised:
26
01
2022
received:
21
05
2021
accepted:
06
02
2022
pubmed:
15
2
2022
medline:
15
4
2022
entrez:
14
2
2022
Statut:
ppublish
Résumé
Acid-sensing ion channels (ASICs) participate in synaptic transmission due to the acidic content of synaptic vesicles, but their contribution to postsynaptic currents is small. This has stimulated attempts to find endogenous ASIC potentiators that could enhance ASIC-mediated currents to physiologically relevant values. Here we demonstrate that glutamate, which serves as a neurotransmitter, potentiates recombinant ASIC1a in the submillimolar concentration range. The effect of glutamate is especially interesting as ASIC's presence has been shown in glutamatergic synapses. At pH=6.5 glutamate had maximum potentiation of 87% with an EC
Substances chimiques
Acid Sensing Ion Channels
0
Glutamic Acid
3KX376GY7L
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e22227Informations de copyright
© 2022 Wiley Periodicals LLC.
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