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Updated: Jun 12, 2026

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Published on: February 11, 2021
Action potential-enhanced ATP release from taste cells through hemichannels
Yoshihiro Murata1, Toshiaki Yasuo, Ryusuke Yoshida
1Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University, Higashi-ku, Fukuoka, Japan.
Action potentials in taste cells enhance adenosine triphosphate (ATP) release, particularly for sweet, bitter, and umami tastes. This release is mediated by pannexin 1 channels, not connexin hemichannels.
Area of Science:
- Neuroscience
- Sensory Biology
- Cell Biology
Background:
- Type II taste cells, crucial for detecting sweet, bitter, and umami tastes, express numerous transduction molecules.
- The functional role of action potentials in Type II taste cells is unclear due to their poorly developed synapses.
Purpose of the Study:
- To investigate the relationship between action potentials and adenosine triphosphate (ATP) release from taste cells.
- To determine the specific molecular mechanisms underlying ATP release in response to taste stimuli.
Main Methods:
- Utilized mice expressing green fluorescent protein (GFP) under the alpha-gustducin promoter to identify Type II taste cells.
- Recorded action potentials from single GFP-positive taste cells using basolateral electrodes.
- Quantified ATP release via a luciferase assay in the collected electrode solution following tastant stimulation.
Main Results:
- Sweet, bitter, and umami tastant stimulation increased ATP release, with higher release correlating with increased firing rates.
- Elevated spontaneous action potential firing rates also triggered ATP release.
- Tetrodotoxin depressed ATP release, while carbenoxolone inhibited it, supporting a role for pannexin 1 channels.
Conclusions:
- Action potentials in taste cells significantly enhance ATP release in response to sweet, bitter, and umami stimuli.
- Pannexin 1 channels, rather than connexin-based hemichannels, mediate this action potential-dependent ATP release.
- These findings clarify a key mechanism in taste signal transduction.
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