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

Research output: Contribution to journalArticle

22 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 languageEnglish
Article number13791
JournalNature communications
Volume7
DOIs
Publication statusPublished - 2016 Dec 19

ASJC Scopus subject areas

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

Fingerprint Dive into the research topics of 'The Ca<sup>2+</sup> -activated chloride channel anoctamin-2 mediates spike-frequency adaptation and regulates sensory transmission in thalamocortical neurons'. Together they form a unique fingerprint.

Cite this