Mice deficient in TWIK-1 are more susceptible to kainic acid-induced seizures

Ajung Kim, Yeonju Bae, Changdev G. Gadhe, Hyun Gug Jung, Esther Yang, Hyun Kim, Jaekwang Lee, Chanseob Shim, Young Hoon Sung, Junyeol Noh, Eun Jin Kim, Dawon Kang, Ae Nim Pae, Eun Mi Hwang, Jae Yong Park

Research output: Contribution to journalArticlepeer-review

Abstract

TWIK-1 belongs to the two-pore domain K+ (K2P) channel family, which plays an essential role in the background K+ conductance of cells. Despite the development of exon 2-deleted Twik-1 knockout (KO) mice, the physiological role of TWIK-1 has remained largely unknown. Here, we observed that the exon 2-deleted Twik-1 KO mice expressed an internally deleted TWIK-1 (TWIK-1 ΔEx2) protein, which unexpectedly acts as a functional K+ channel. The Twik-1 nKO mice in which exon 1 was targeted using the CRISPR-Cas9 technique provides strong evidence that TWIK-1 mediates K+ currents that are responsible for the background passive conductance in astrocytes. Deficiency of TWIK-1-mediated astrocytic passive conductance increased susceptibility to kainic acid-induced seizures. This study paves the way for functional studies on TWIK-1-mediated astrocytic passive conductance. In addition, the exon 1-targeted Twik-1 KO mice would help elucidate the physiological roles of TWIK-1.

Original languageEnglish
Article number111587
JournaliScience
Volume28
Issue number1
DOIs
Publication statusPublished - 2025 Jan 17

Bibliographical note

Publisher Copyright:
© 2024 The Author(s)

Keywords

  • Biological sciences
  • Molecular neuroscience
  • Natural sciences
  • Neuroscience
  • Systems neuroscience

ASJC Scopus subject areas

  • General

Fingerprint

Dive into the research topics of 'Mice deficient in TWIK-1 are more susceptible to kainic acid-induced seizures'. Together they form a unique fingerprint.

Cite this