Acetylcholine is released from taste cells, enhancing taste signalling
Acetylcholine is released from taste cells, enhancing taste signalling
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DOI：
10.1113/jphysiol.2012.232009
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发表时间：
2012-07-01
影响因子：
5.5
通讯作者：
Roper, Stephen D.
中科院分区：
文献类型：
--
作者：
Dando, Robin;Roper, Stephen D.
关键点乙酰胆碱（Acetylcholine，ACh）是一种经典的神经递质，刺激受体（II型）味蕾细胞上的M3毒蕈碱受体。这种毒蕈碱自分泌反馈放大了味觉诱发的Ca 2+信号，并增强了从受体（II型）细胞释放的传入神经递质（ATP）。缺乏M3毒蕈碱受体的小鼠的味觉受体细胞显示出对味觉刺激的敏感性降低。这一发现强调了味蕾中的一种新的信号通路，并可能解释与某些抗胆碱能药物相关的味觉障碍（即副作用）。摘要乙酰胆碱（Acetylcholine，ACh）是一种与味蕾有关的候选神经递质，可促进II型味觉细胞的钙离子动员。使用RT-PCR分析和药理学干预，我们表明，毒蕈碱乙酰胆碱受体M3介导这些行动。ACh可增强味觉感受器细胞的Ca ~（2+）反应和ATP的分泌。阻断毒蕈碱受体可抑制受体细胞的味觉诱发反应，表明乙酰胆碱在味觉刺激过程中通常从味觉细胞释放。乙酰胆碱生物传感器证实，的确，味觉受体细胞分泌乙酰胆碱在味觉刺激。毒蕈碱受体的基因缺失导致味蕾的ATP分泌显著减少。这些数据证明了乙酰胆碱作为味蕾递质的新作用。我们的研究结果特别暗示，乙酰胆碱是一种自分泌递质分泌的味觉感受器细胞在味觉刺激，增强味觉诱发的反应和传入递质分泌。
Key points Acetylcholine (ACh), a classical neurotransmitter, stimulates M3 muscarinic receptors on Receptor (Type II) taste bud cells ACh is synthesized by, and released from Receptor (Type II) taste bud cells during gustatory stimulation. This muscarinic autocrine feedback amplifies taste-evoked Ca2+ signals and enhances afferent neurotransmitter (ATP) release from Receptor (Type II) cells. Taste Receptor cells in mice lacking M3 muscarinic receptors display depressed sensitivity to gustatory stimulation The findings highlight a new signalling pathway in taste buds and may explain taste disturbances (i.e. side effects) associated with certain anticholinergic drugs. Abstract Acetylcholine (ACh), a candidate neurotransmitter that has been implicated in taste buds, elicits calcium mobilization in Receptor (Type II) taste cells. Using RT-PCR analysis and pharmacological interventions, we demonstrate that the muscarinic acetylcholine receptor M3 mediates these actions. Applying ACh enhanced both taste-evoked Ca2+ responses and taste-evoked afferent neurotransmitter (ATP) secretion from taste Receptor cells. Blocking muscarinic receptors depressed taste-evoked responses in Receptor cells, suggesting that ACh is normally released from taste cells during taste stimulation. ACh biosensors confirmed that, indeed, taste Receptor cells secrete acetylcholine during gustatory stimulation. Genetic deletion of muscarinic receptors resulted in significantly diminished ATP secretion from taste buds. The data demonstrate a new role for acetylcholine as a taste bud transmitter. Our results imply specifically that ACh is an autocrine transmitter secreted by taste Receptor cells during gustatory stimulation, enhancing taste-evoked responses and afferent transmitter secretion.