Abstract:
:Recognition of sweet, bitter and umami tastes requires the non-vesicular release from taste bud cells of ATP, which acts as a neurotransmitter to activate afferent neural gustatory pathways. However, how ATP is released to fulfil this function is not fully understood. Here we show that calcium homeostasis modulator 1 (CALHM1), a voltage-gated ion channel, is indispensable for taste-stimuli-evoked ATP release from sweet-, bitter- and umami-sensing taste bud cells. Calhm1 knockout mice have severely impaired perceptions of sweet, bitter and umami compounds, whereas their recognition of sour and salty tastes remains mostly normal. Calhm1 deficiency affects taste perception without interfering with taste cell development or integrity. CALHM1 is expressed specifically in sweet/bitter/umami-sensing type II taste bud cells. Its heterologous expression induces a novel ATP permeability that releases ATP from cells in response to manipulations that activate the CALHM1 ion channel. Knockout of Calhm1 strongly reduces voltage-gated currents in type II cells and taste-evoked ATP release from taste buds without affecting the excitability of taste cells by taste stimuli. Thus, CALHM1 is a voltage-gated ATP-release channel required for sweet, bitter and umami taste perception.
journal_name
Naturejournal_title
Natureauthors
Taruno A,Vingtdeux V,Ohmoto M,Ma Z,Dvoryanchikov G,Li A,Adrien L,Zhao H,Leung S,Abernethy M,Koppel J,Davies P,Civan MM,Chaudhari N,Matsumoto I,Hellekant G,Tordoff MG,Marambaud P,Foskett JKdoi
10.1038/nature11906subject
Has Abstractpub_date
2013-03-14 00:00:00pages
223-6issue
7440eissn
0028-0836issn
1476-4687pii
nature11906journal_volume
495pub_type
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