The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.

Details

Ressource 1Download: BIB_52266DFA56FD.P001.pdf (1650.70 [Ko])
State: Public
Version: Author's accepted manuscript
Secondary document(s)
Download: Boscardin_ENaC-ASIC_review_post-print.pdf (5131.54 [Ko])
State: Public
Version: author
Serval ID
serval:BIB_52266DFA56FD
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Title
The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.
Journal
British Journal of Pharmacology
Author(s)
Boscardin E., Alijevic O., Hummler E., Frateschi S., Kellenberger S.
ISSN
1476-5381 (Electronic)
ISSN-L
0007-1188
Publication state
Published
Issued date
09/2016
Peer-reviewed
Oui
Volume
173
Number
18
Pages
2671-2701
Language
english
Notes
Publication types: Journal Article ; ReviewPublication Status: ppublish
Abstract
Acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC) are both members of the ENaC/degenerin family of amiloride-sensitive Na(+) channels. ASICs act as proton sensors in the nervous system where they contribute, besides other roles, to fear behaviour, learning and pain sensation. ENaC mediates Na(+) reabsorption across epithelia of the distal kidney and colon and of the airways. ENaC is a clinically used drug target in the context of hypertension and cystic fibrosis, while ASIC is an interesting potential target. Following a brief introduction, here we will review selected aspects of ASIC and ENaC function. We discuss the origin and nature of pH changes in the brain and the involvement of ASICs in synaptic signalling. We expose how in the peripheral nervous system, ASICs cover together with other ion channels a wide pH range as proton sensors. We introduce the mechanisms of aldosterone-dependent ENaC regulation and the evidence for an aldosterone-independent control of ENaC activity, such as regulation by dietary K(+) . We then provide an overview of the regulation of ENaC by proteases, a topic of increasing interest over the past few years. In spite of the profound differences in the physiological and pathological roles of ASICs and ENaC, these channels share many basic functional and structural properties. It is likely that further research will identify physiological contexts in which ASICs and ENaC have similar or overlapping roles.
Pubmed
Open Access
Yes
Create date
18/06/2016 18:59
Last modification date
20/08/2019 15:07
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