The Ca2+-activated chloride channel anoctamin-2 mediates spike-frequency adaptation and regulates sensory transmission in thalamocortical neurons

Go Eun Ha, Jaekwang Lee, Hankyul Kwak, Kiyeong Song, Jea Kwon, Soon-Young Jung, Joohyeon Hong, Gyeong-Eon Chang, Eun Mi Hwang, Hee-Sup Shin, C. Justin Lee and Eunji Cheong ()
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Go Eun Ha: College of Life Science and Biotechnology, Yonsei University
Jaekwang Lee: Center for Neural Science, Korea Institute of Science and Technology
Hankyul Kwak: College of Life Science and Biotechnology, Yonsei University
Kiyeong Song: College of Life Science and Biotechnology, Yonsei University
Jea Kwon: Center for Neural Science, Korea Institute of Science and Technology
Soon-Young Jung: Center for Neural Science, Korea Institute of Science and Technology
Joohyeon Hong: College of Life Science and Biotechnology, Yonsei University
Gyeong-Eon Chang: College of Life Science and Biotechnology, Yonsei University
Eun Mi Hwang: Center for Functional Connectomics, Korea Institute of Science and Technology
Hee-Sup Shin: Center for Cognition and Sociality, Institute for Basic Science
C. Justin Lee: Center for Neural Science, Korea Institute of Science and Technology
Eunji Cheong: College of Life Science and Biotechnology, Yonsei University

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract 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.

Date: 2016
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DOI: 10.1038/ncomms13791

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