| First Author | Xu Y | Year | 2020 |
| Journal | Mol Brain | Volume | 13 |
| Issue | 1 | Pages | 132 |
| PubMed ID | 32993733 | Mgi Jnum | J:361295 |
| Mgi Id | MGI:6766102 | Doi | 10.1186/s13041-020-00672-8 |
| Citation | Xu Y, et al. (2020) GPR68 deletion impairs hippocampal long-term potentiation and passive avoidance behavior. Mol Brain 13(1):132 |
| abstractText | 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. |
