Acetylcholine is released from taste cells, enhancing taste signalling

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.