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Alpha-melanocyte-stimulating hormone ( α -MSH) is processed from proopiomelanocortin (POMC) and acts on the melanocortin receptors, MC3 and MC4.  α -MSH plays a key role in energy homeostasis. In the present study, to shed light on the mechanisms by which  α -MSH exerts its anorectic effects, extracellular neuronal activity was recorded in the hypothalamus and the dorsal vagal complex (DVC) of anesthetized rats. We examined the impact of  α -MSH on glucose-sensing neurons and gastric distension (GD) sensitive neurons. In the lateral hypothalamus (LHA),  α -MSH inhibited 75.0% of the glucose-inhibited (GI) neurons. In the ventromedial nucleus (VMN), most glucose-sensitive neurons were glucose-excited (GE) neurons, which were mainly activated by  α -MSH. In the paraventricular nucleus (PVN),  α -MSH suppressed the majority of GI neurons and excited most GE neurons. In the DVC, among the 20 GI neurons examined for a response to  α -MSH, 1 was activated, 16 were depressed, and 3 failed to respond. Nineteen of 24 GE neurons were activated by  α -MSH administration. Additionally, among the 42 DVC neurons examined for responses to GD, 23 were excited (GD-EXC) and 19 were inhibited (GD-INH). Fifteen of 20 GD-EXC neurons were excited, whereas 11 out of 14 GD-INH neurons were suppressed by  α -MSH. All these responses were abolished by pretreatment with the MC3/4R antagonist, SHU9119. In conclusion, the activity of glucose-sensitive neurons and GD-sensitive neurons in the hypothalamus and DVC can be modulated by  α -MSH.

α-MSH Influences the Excitability of Feeding-Related Neurons in the Hypothalamus and Dorsal Vagal Complex of Rats