The Ca2+-activated chloride channel anoctamin-2 mediates spike-frequency adaptation and regulates sensory transmission in thalamocortical neurons.
- The Ca2+-activated chloride channel anoctamin-2 mediates spike-frequency adaptation and regulates sensory transmission in thalamocortical neurons.
- 이창준; 황은미; 권재; Go Eun Ha; Jaekwang Lee; Hankyul Kwak; Kiyeong Song; Soon-Young Jung; Joohyeon Hong; Gyeong-Eon Chang; Hee-Sup Shin; Eunji Cheong
- Issue Date
- Nature Communications
- VOL 7-13791-13
- Neuronal ﬁ ring 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 Ca2þ-activated Cl channel (CACC) anoctamin-2 (ANO2). Knockdown of ANO2 in TC neurons results in signiﬁ cantly reduced spike-frequency adaptation along with increased tonic spiking. Moreover, thalamusspeciﬁ c 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.
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