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Nat Commun. 2016 Dec 19;7:13791. doi: 10.1038/ncomms13791.

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

Author information

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.

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.

PMID:
27991499
PMCID:
PMC5187435
DOI:
10.1038/ncomms13791
[Indexed for MEDLINE]
Free PMC Article

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