| First Author | Ha GE | Year | 2016 |
| Journal | Nat Commun | Volume | 7 |
| Pages | 13791 | PubMed ID | 27991499 |
| Mgi Jnum | J:243451 | Mgi Id | MGI:5908504 |
| Doi | 10.1038/ncomms13791 | Citation | Ha GE, et al. (2016) The Ca2+-activated chloride channel anoctamin-2 mediates spike-frequency adaptation and regulates sensory transmission in thalamocortical neurons. Nat Commun 7:13791 |
| abstractText | Neuronal firing patterns, which are crucial for determining the nature of encoded information, have been widely studied; however, the molecular identity and cellular mechanisms of spike-frequency adaptation are still not fully understood. Here we show that spike-frequency adaptation in thalamocortical (TC) neurons is mediated by the Ca2+-activated Cl- channel (CACC) anoctamin-2 (ANO2). Knockdown of ANO2 in TC neurons results in significantly reduced spike-frequency adaptation along with increased tonic spiking. Moreover, thalamus-specific knockdown of ANO2 increases visceral pain responses. These results indicate that ANO2 contributes to reductions in spike generation in highly activated TC neurons and thereby restricts persistent information transmission. |
