GPR68 deletion impairs hippocampal long-term potentiation and passive avoidance behavior

Molecular Brain

Mike T. Lin¹  Xiang-ming Zha¹  Yuanyuan Xu¹ 

[1] Department of Physiology and Cell Biology, University of South Alabama College of Medicine, 5851 USA Dr. N, MSB3074, 36688, Mobile, AL, USA;

关键词: OGR1;    Synaptic plasticity;    Fear memory;   

DOI  :  10.1186/s13041-020-00672-8

来源: Springer

【 摘 要 】

Increased neural activities reduced pH at the synaptic cleft and interstitial spaces. Recent studies have shown that protons function as a neurotransmitter. However, it remains unclear whether protons signal through a metabotropic receptor to regulate synaptic function. Here, we showed that GPR68, a proton-sensitive GPCR, exhibited wide expression in the hippocampus, with higher expression observed in CA3 pyramidal neurons and dentate granule cells. In organotypic hippocampal slice neurons, ectopically expressed GPR68-GFP was present in dendrites, dendritic spines, and axons. Recordings in hippocampal slices isolated from GPR68−/− mice showed a reduced fiber volley at the Schaffer collateral-CA1 synapses, a reduced long-term potentiation (LTP), but unaltered paired-pulse ratio. In a step-through passive avoidance test, GPR68−/− mice exhibited reduced avoidance to the dark chamber. These findings showed that GPR68 contributes to hippocampal LTP and aversive fear memory.

【 授权许可】

CC BY