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; Eunji Cheong

doi:10.1038/ncomms13791

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, Eunji Cheong

KU-KIST Graduate School of Converging Science and Technology

Research output: Contribution to journal › Article › peer-review

38 Citations (Scopus)

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.

Original language	English
Article number	13791
Journal	Nature communications
Volume	7
DOIs	https://doi.org/10.1038/ncomms13791
Publication status	Published - 2016 Dec 19

ASJC Scopus subject areas

Chemistry(all)
Biochemistry, Genetics and Molecular Biology(all)
Physics and Astronomy(all)

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

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.",

author = "Ha, {Go Eun} and Jaekwang Lee and Hankyul Kwak and Kiyeong Song and Jea Kwon and Jung, {Soon Young} and Joohyeon Hong and Chang, {Gyeong Eon} and Hwang, {Eun Mi} and Shin, {Hee Sup} and Lee, {C. Justin} and Eunji Cheong",

note = "Funding Information: This research was supported by the National Research Foundation (NRF-2014R1A2A2A01006940, NRF2015R1A3A2066619 and NRF-2014M3A7 B4051596), funded by the government of the Republic of Korea (Ministry of Science, ICT and Future Planning, MSIP), International Collaborative R&D Program, funded by the Ministry of Trade, Industry and Energy (MOTIE, Korea), the Yonsei University Future-Leading Research Initiative of 2015 (2015-22-0163), KIST Institutional Program (2E26664), Samsung Research Funding Center of Samsung Electronics under Project Number SRFC-IT1402-08 and the Brain Korea 21 (BK21) PLUS program. G.E.H., H.K., G.-E.C. and J.H. are fellowship awardee by the BK21 PLUS program. Publisher Copyright: {\textcopyright} The Author(s) 2016.",

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day = "19",

doi = "10.1038/ncomms13791",

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T1 - The Ca2+ -activated chloride channel anoctamin-2 mediates spike-frequency adaptation and regulates sensory transmission in thalamocortical neurons

AU - Ha, Go Eun

AU - Lee, Jaekwang

AU - Kwak, Hankyul

AU - Song, Kiyeong

AU - Kwon, Jea

AU - Jung, Soon Young

AU - Hong, Joohyeon

AU - Chang, Gyeong Eon

AU - Hwang, Eun Mi

AU - Shin, Hee Sup

AU - Lee, C. Justin

AU - Cheong, Eunji

N1 - Funding Information: This research was supported by the National Research Foundation (NRF-2014R1A2A2A01006940, NRF2015R1A3A2066619 and NRF-2014M3A7 B4051596), funded by the government of the Republic of Korea (Ministry of Science, ICT and Future Planning, MSIP), International Collaborative R&D Program, funded by the Ministry of Trade, Industry and Energy (MOTIE, Korea), the Yonsei University Future-Leading Research Initiative of 2015 (2015-22-0163), KIST Institutional Program (2E26664), Samsung Research Funding Center of Samsung Electronics under Project Number SRFC-IT1402-08 and the Brain Korea 21 (BK21) PLUS program. G.E.H., H.K., G.-E.C. and J.H. are fellowship awardee by the BK21 PLUS program. Publisher Copyright: © The Author(s) 2016.

PY - 2016/12/19

Y1 - 2016/12/19

N2 - 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.

AB - 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.

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

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