西亚试剂：CALHM1 ion channel mediates purinergic neurotransmission of

CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes

Akiyuki Taruno, Valérie Vingtdeux, Makoto Ohmoto, Zhongming Ma,Gennady Dvoryanchikov, Ang Li, Leslie Adrien, Haitian Zhao, Sze Leung,Maria Abernethy, Jeremy Koppel, Peter Davies, Mortimer M-Civan, Nirupa Chaudhari, Ichiro Matsumoto,Goran Hellekant, Michael G-Tordoff, Philippe Marambaud & J-Kevin Foskett.

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 pathways1. 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 channel2, 3, 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

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