| Literature DB >> 32553165 |
Yulin Zhao1, Peter Man-Un Ung2, Gergely Zahoránszky-Kőhalmi3, Alexey V Zakharov3, Natalia J Martinez3, Anton Simeonov3, Ian W Glaaser1, Ganesha Rai3, Avner Schlessinger2, Juan J Marugan3, Paul A Slesinger4.
Abstract
G-protein-gated inwardly rectifying K+ (GIRK) channels are essential effectors of inhibitory neurotransmission in the brain. GIRK channels have been implicated in diseases with abnormal neuronal excitability, including epilepsy and addiction. GIRK channels are tetramers composed of either the same subunit (e.g., homotetramers) or different subunits (e.g., heterotetramers). Compounds that specifically target subsets of GIRK channels in vivo are lacking. Previous studies have shown that alcohol directly activates GIRK channels through a hydrophobic pocket located in the cytoplasmic domain of the channel. Here, we report the identification and functional characterization of a GIRK1-selective activator, termed GiGA1, that targets the alcohol pocket. GiGA1 activates GIRK1/GIRK2 both in vitro and in vivo and, in turn, mitigates the effects of a convulsant in an acute epilepsy mouse model. These results shed light on the structure-based development of subunit-specific GIRK modulators that could provide potential treatments for brain disorders.Entities:
Keywords: G-protein-gated inwardly rectifying K(+) channel; GIRK1-selective activator; alcohol-like kinetics; antiseizure; epilepsy
Mesh:
Substances:
Year: 2020 PMID: 32553165 PMCID: PMC7401321 DOI: 10.1016/j.celrep.2020.107770
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423