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How do taste cells lacking synapses mediate neurotransmission? <scp>CALHM</scp>1, a voltage‐gated <scp>ATP</scp> channel

Akiyuki TarunoDepartment of Molecular Cell Physiology Kyoto Prefectural University of Medicine Kyoto JapanIchiro MatsumotoMonell Chemical Senses Center Philadelphia PA USAZhongming MaDepartment of Physiology University of Pennsylvania Philadelphia PA USAPhilippe MarambaudLitwin‐Zucker Research Center for the Study of Alzheimer's Disease The Feinstein Institute for Medical Research Manhasset NY USAJ. Kevin FoskettDepartment of Cell and Developmental Biology University of Pennsylvania Philadelphia PA USA
2013en
ABI

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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. Calhm1 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. Calhm1 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.

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