Abstract
Glutamate is the neurotransmitter responsible for fast excitatory transmission from vagal afferents to second order neurons in the NTS. Antagonism of NMDA-type glutamate receptors in the NTS increases food intake and attenuates reduction of food intake by vagally mediated satiation signals, such as cholecystokinin. Although, the cellular location(s) of NMDA receptors that participate in satiation is uncertain, recent findings suggest that attenuation of satiation by NMDA receptor antagonists is due, at least in part, to their action on primary vagal afferents themselves. While evidence is accumulating that NMDA receptors located on vagal afferent endings in the hindbrain are involved in control of food intake, there also is preliminary evidence that peripheral NMDA receptors also may influence vagal control of food intake. Hence, NMDA receptor expression on central and perhaps peripheral vagal afferent endings could provide a parsimonious mechanism for modulation of satiation signals by endogenously released glutamate.