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Satiation and masticatory function modulated by brain histamine in rats
T Fujise1, H Yoshimatsu, M Kurokawa
1Department of Pediatric Dentistry, Faculty of Dentistry, Kyushu University 61, Fukuoka, Japan.
Summary
Histamine (HA) in the brain influences satiety. Depleting HA in the mesencephalic trigeminal sensory nucleus (Me5) slows eating, while depletion in the ventromedial hypothalamus (VMH) increases meal size, both prolonging duration.
Area of Science:
- Neuroscience
- Neuroendocrinology
- Behavioral Neuroscience
Background:
- Histaminergic neurons densely innervate the ventromedial hypothalamus (VMH) and mesencephalic trigeminal sensory nucleus (Me5).
- Neuronal histamine (HA) plays a role in regulating feeding behavior and satiety signals.
Purpose of the Study:
- To investigate the specific roles of the VMH and Me5 in HA-mediated satiety.
- To elucidate the temporal dynamics of HA turnover in response to feeding cues.
Main Methods:
- Bilateral microinfusion of alpha-fluoromethylhistidine (FMH) to deplete neuronal HA in the Me5.
- Assessment of feeding parameters (speed, duration, size) after HA depletion.
- Measurement of HA turnover rates in the VMH and Me5 regions.
- Gastric intubation of liquid diet or water to assess satiety signal influence.
Main Results:
- Me5 HA depletion reduced eating speed and prolonged meal duration, without affecting meal size.
- VMH HA depletion increased meal size and prolonged duration, but not eating speed.
- HA turnover increased in the Me5 region earlier than in the hypothalamus post-feeding.
- Gastric intubation abolished HA turnover increases in both regions, indicating satiety signal involvement.
Conclusions:
- Brain HA modulates satiation via both the VMH and masticatory pathways involving the Me5.
- Mastication activates HA signaling earlier in the Me5 and later in the hypothalamus.
- Satiety signals from oral proprioceptors initiated by chewing influence HA function in these brain regions.