How do taste cells lacking synapses mediate neurotransmission? CALHM1, a voltage‐gated ATP channel. (17th September 2013)

• Record Type: Journal Article
• Authors: Taruno, Akiyuki; Matsumoto, Ichiro; Ma, Zhongming; Marambaud, Philippe; Foskett, J. Kevin
• Is Part Of: BioEssays. Volume 35:Number 12(2013:Dec.)
• Page Start: 1111
• Page End: 1118
• Publication Date: 2013-09-17
• Subjects: Molecular biology -- Periodicals; Cytology -- Periodicals; Developmental biology -- Periodicals; 572.8
• DOI: 10.1002/bies.201300077
• Languages: English
• ISSNs: 0265-9247

Abstract

<abstract abstract-type="main" xml:lang="en"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="bies201300077-sec-0001" sec-type="section"> <p>CALHM1 was recently demonstrated to be a voltage‐gated ATP‐permeable ion channel and to serve as a bona fide conduit for ATP release from sweet‐, umami‐, and bitter‐sensing type II taste cells. <italic>Calhm1</italic> is expressed in taste buds exclusively in type II cells and its product has structural and functional similarities with connexins and pannexins, two families of channel protein candidates for ATP release by type II cells. <italic>Calhm1</italic> knockout in mice leads to loss of perception of sweet, umami, and bitter compounds and to impaired gustatory nerve responses to these tastants. These new studies validate the concept of ATP as the primary neurotransmitter from type II cells to gustatory neurons. Furthermore, they identify voltage‐gated ATP release through CALHM1 as an essential molecular mechanism of ATP release in taste buds. We discuss these new findings, as well as unresolved issues in peripheral taste signaling that we hope will stimulate future research.</p> </sec> </abstract>