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GPR68 deletion impairs hippocampal long-term potentiation and passive avoidance behavior
Yuanyuan Xu1, Mike T Lin1, Xiang-Ming Zha2
1Department of Physiology and Cell Biology, University of South Alabama College of Medicine, 5851 USA Dr. N, MSB3074, Mobile, AL, 36688, USA.
Protons act as neurotransmitters, and G protein-coupled receptor 68 (GPR68) is crucial for synaptic plasticity and memory. GPR68 deficiency impairs long-term potentiation and fear memory in mice.
Area of Science:
- Neuroscience
- Molecular Biology
- Neurochemistry
Background:
- Neural activity lowers pH in synaptic clefts and interstitial spaces.
- Recent research suggests protons function as neurotransmitters.
- The role of metabotropic receptors in proton signaling remains unclear.
Purpose of the Study:
- To investigate if GPR68, a proton-sensitive GPCR, mediates proton signaling in the hippocampus.
- To determine GPR68's role in synaptic function, long-term potentiation (LTP), and fear memory.
Main Methods:
- Examined GPR68 expression in hippocampal neurons.
- Performed electrophysiological recordings in GPR68 knockout (GPR68-/-) mice.
- Assessed fear memory using a step-through passive avoidance test.
Main Results:
- GPR68 is widely expressed in the hippocampus, particularly in CA3 pyramidal neurons and dentate granule cells.
- GPR68-/- mice showed reduced synaptic fiber volley and impaired LTP at Schaffer collateral-CA1 synapses.
- GPR68 deficiency led to reduced avoidance in a fear memory test.
Conclusions:
- GPR68 is a key mediator of proton signaling in the hippocampus.
- GPR68 plays a significant role in hippocampal long-term potentiation.
- GPR68 is essential for aversive fear memory formation.
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