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* To whom correspondence should be addressed. E-mail: kannanh{at}post.miyazaki-med.ac.jp.
The effect of neuromedin U (NMU) on rat paraventricular nucleus (PVN) neurons was examined using whole-cell patch-clamp recordings. Under current-clamp, 31% of PVN pavocellular neurons (n = 243) were depolarized by 100 nM NMU, but magnocellular neurons were not affected. NMU (10 nM to 1µM) resulted in increased basal firing rate and depolarization in a dose-dependent manner with an EC50 of 70 nM. NMU-induced depolarization was unaffected by co-perfusion with 0.5µM tetrodotoxin (TTX) + 10µM CNQX + 10µM bicuculline. Extracellular application of 70µM ZD 7288 completely inhibited NMU-induced depolarization. Under voltage-clamp, 1µM NMU produced negligible inward current but did increase the hyperpolarization-activated current (IH) at step potentials less than -80 mV. The effects of NMU on IH were voltage-dependent, and NMU shifted the IH conductance-voltage relationship (V1/2) by about 10.8 mV and enhanced IH kinetics without changing the slope constant (k). Extracellular application of 70µM ZD 7288 or 3 mM Cs+ blocked IH and the effects of NMU in voltage-clamp. These results suggest that NMU selectively depolarizes the subpopulation of PVN pavocellular via enhancement of the hyperpolarization-activated inward current.
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