| First Author | Nomura K | Year | 2020 |
| Journal | Neuron | Volume | 106 |
| Issue | 5 | Pages | 816-829.e6 |
| PubMed ID | 32229307 | Mgi Jnum | J:298578 |
| Mgi Id | MGI:6449522 | Doi | 10.1016/j.neuron.2020.03.006 |
| Citation | Nomura K, et al. (2020) All-Electrical Ca(2+)-Independent Signal Transduction Mediates Attractive Sodium Taste in Taste Buds. Neuron 106(5):816-829.e6 |
| abstractText | Sodium taste regulates salt intake. The amiloride-sensitive epithelial sodium channel (ENaC) is the Na(+) sensor in taste cells mediating attraction to sodium salts. However, cells and intracellular signaling underlying sodium taste in taste buds remain long-standing enigmas. Here, we show that a subset of taste cells with ENaC activity fire action potentials in response to ENaC-mediated Na(+) influx without changing the intracellular Ca(2+) concentration and form a channel synapse with afferent neurons involving the voltage-gated neurotransmitter-release channel composed of calcium homeostasis modulator 1 (CALHM1) and CALHM3 (CALHM1/3). Genetic elimination of ENaC in CALHM1-expressing cells as well as global CALHM3 deletion abolished amiloride-sensitive neural responses and attenuated behavioral attraction to NaCl. Together, sodium taste is mediated by cells expressing ENaC and CALHM1/3, where oral Na(+) entry elicits suprathreshold depolarization for action potentials driving voltage-dependent neurotransmission via the channel synapse. Thus, all steps in sodium taste signaling are voltage driven and independent of Ca(2+) signals. This work also reveals ENaC-independent salt attraction. |
