Regulation of brain function by thermo-sensor

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I found hippocampus strongly expressed TRPV4 in addition to choloid plexus, where TRPV4 expression was been reported. I considered that body temperature activates brain TRPV4, and the activation might contribute to depolarization of the resting membrane potential (RMP). I compared the RMP between wild-type and TRPV4-deficient neurons at 37℃, and found the wild-type RMP was approximately 5 mV more depolarized than the TRPV4-deficient RMP. I also performed current-injection experiments in both neurons, and found that TRPV4-deficient neurons required much bigger currents to get their firing. Furthermore, I found that glutamate-induced Ca^<2+> influx in wild-type neurons was much bigger than that in TRPV4-deficient neurons at 37℃. APV (a blocker of NMDA receptors) inhibited the enhancement of glutamate-induced Ca^<2+> influx in wild-type neurons at 37℃, suggesting that body temperature depolarized RMP near the thresholds for NMDA receptor activation compared with room temperature condition. Therefore, I conclude that TRPV4 is activated by body temperature in hippocampus, and produces proper environments for their firing.