The Ca2+-activated chloride channel anoctamin-2 mediates spike-frequency adaptation and regulates sensory transmission in thalamocortical neurons
Go Eun Ha1,*, Jaekwang Lee2,*, Hankyul Kwak1, Kiyeong Song1, Jea Kwon2, Soon-Young Jung2, Joohyeon Hong1, Gyeong-Eon Chang1, Eun Mi Hwang3, Hee-Sup Shin4, C. Justin Lee2 & Eunji Cheong1
1 Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Republic of Korea. 2 Center for Neural Science, Korea Institute of Science and Technology, Seoul 02792, Republic of Korea. 3 Center for Functional Connectomics, Korea Institute of Science and Technology, Seoul 02792, Republic of Korea. 4 Center for Cognition and Sociality, Institute for Basic Science, Daejeon 34141, Republic of Korea.
* These authors contributed equally to this work.
Correspondence to Eunji Cheong
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.