SATIATION AND MASTICATORY FUNCTION MODULATED BY BRAIN HISTAMINE IN RATS

Both the ventromedial hypothalamus (VMH) and the mesencephalic trigemi nal sensory nucleus (Me5) are densely innervated by histaminergic neur ons, The depletion of neuronal histamine (HA) from the Me5 by the bila teral 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 a nd prolonged its duration, but not the eating speed, When the HA turno ver rate was measured at 15 min after the scheduled feeding following fasting for less than 24 hr, the rate increased in the region includin g the Me5, but not in the hypothalamus. The turnover rate reached high er levels at 60 min in both regions, Gastric intubation of an isocalor ic liquid diet or an equivolume of water with the liquid diet abolishe d the increase in HA turnover both in the Me5 region and the hypothala mus. The present findings indicate that brain HA thus modulates satiat ion through both the VMH and masticatory function as well as due to th e action of the Me5, The HA function activated by mastication began ea rlier in the Me5 and later in the hypothalamus due to a signal origina ting from the oral proprioceptors and initiated by chewing.