Satiation and masticatory function modulated by brain histamine in rats.

Abstract

Both the ventromedial hypothalamus (VMH) and the mesencephalic trigeminal sensory nucleus (Me5) are densely innervated by histaminergic neurons. The depletion of neuronal histamine (HA) from the Me5 by the bilateral microinfusion of 448 nmol/rat alpha-fluoromethylhistidine (FMH), a specific suicide inhibitor of histidine decarboxylase, reduced the eating speed and prolonged meal duration, while leaving the meal size unaffected. HA depletion from the VMH increased the size of the meal and prolonged its duration, but not the eating speed. When the HA turnover rate was measured at 15 min after the scheduled feeding following fasting for less than 24 hr, the rate increased in the region including the Me5, but not in the hypothalamus. The turnover rate reached higher levels at 60 min in both regions. Gastric intubation of an isocaloric liquid diet or an equivolume of water with the liquid diet abolished the increase in HA turnover both in the Me5 region and the hypothalamus. The present findings indicate that brain HA thus modulates satiation through both the VMH and masticatory function as well as due to the action of the Me5. The HA function activated by mastication began earlier in the Me5 and later in the hypothalamus due to a signal originating from the oral proprioceptors and initiated by chewing.