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Neuromedin U Depolarizes Rat Hypothalamic Paraventricular Nucleus Neurons In Vitro by Enhancing I_H Channel Activity

¹ Department of Physiology, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; ² Department of Anesthesiology, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; ³ Department of Internal Medicine, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan; ⁴ Department of Public Health, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan

Submitted 10 March 2003; accepted in final form 11 April 2003

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 parvocellular neurons (n = 243) were depolarized by 100 nM NMU, but magnocellular neurons were not affected. NMU (10 nM to 1 µM) 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 0.5 µM TTX + 10 µM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) + 10 µM bicuculline. Extracellular application of 70 µM ZD 7288 completely inhibited NMU-induced depolarization. Under voltage-clamp, 1 µM NMU produced negligible inward current but did increase the hyperpolarization-activated current (I_H) at step potentials less than –80 mV. The effects of NMU on I_H were voltage-dependent, and NMU shifted the I_H conductance-voltage relationship (V_1/2) by about 10.8 mV and enhanced I_H kinetics without changing the slope constant (k). Extracellular application of 70 µM ZD 7288 or 3 mM Cs⁺ blocked I_H and the effects of NMU in voltage-clamp. These results suggest that NMU selectively depolarizes the subpopulation of PVN parvocellular neurons via enhancement of the hyperpolarization-activated inward current.

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