Effect of the N-methyl-d-aspartate receptor antagonist on locomotor activity and cholecystokinin-induced anorexigenic action in a goldfish model

Abstract

We have previously identified that peripherally administered cholecystokinin (CCK) exerts an anorexigenic action via the vagal afferent, and subsequently the brain melanocortin- and corticotropin-releasing hormone-neuronal pathways in goldfish. N-Methyl-d-aspartate (NMDA) receptors have been shown to be involved in the regulations of locomotor activity and food intake in mammals. Although several neuropeptides and other factors exert similar effects in fish and mammals, the role of NMDA receptor in the control of locomotor activity and feeding behavior in fish is still unclear. In the present study, we examined the effect of the NMDA receptor antagonist, MK-801, on locomotor activity and food intake in the goldfish. Intraperitoneal (IP) injection of MK-801 at 0.15nmol/g body weight (BW) increased locomotor activity, but did not affect food consumption. IP injection of MK-801 at same dose attenuated peripheral CCK (100pmol/g BW)-induced anorexigenic, but not peripheral acyl ghrelin (10pmol/g BW)-induced orexigenic actions. These data show for the first time that the NMDA receptor-signaling pathway is involved in the regulation of locomotor activity and feeding behavior through modulation of the peripheral CCK-induced satiety signal, but not the orexigenic effect of ghrelin.