Dv. Sivarao et al., Vagally-regulated gastric motor activity: evidence for kainate and NMDA receptor mediation, EUR J PHARM, 368(2-3), 1999, pp. 173-182
Blockade of GABA(A) receptors in the dorsal vagal complex produces marked g
astric motor excitation. This effect is abolished by a prior microinjection
of a non-selective excitatory amino acid receptor antagonist. Hen we prese
nt functional evidence for kainate and NMDA receptor-mediated gastric excit
ation in the dorsal vagal complex. Microinjections into the dorsal vagal co
mplex were performed in alpha-chloralose-anesthetized rats using multi-barr
elled glass micropipettes while recording intragastric pressure and motilit
y. Kainic acid (30 and 100 pmol in 30 nl) and NMDA (100 and 300 pmol) produ
ced dose-related increases in intragastric pressure and motility. The gastr
ic responses to kainate (30 pmol) and NMDA were selectively abolished by pr
ior microinjection 6,7 -dinitroquinoxaline-2, 3 -dione (600 pmol, 60 nl) an
d DL-2-amino-5-phosphanopentanoic acid (2 nmol), respectively. Atropine (1
mg/kg, i.v.) pretreatment blocked kainate-, NMDA- and l-glutamate-induced g
astric excitation. Thus, both kainate- and NMDA-receptors in the dorsal vag
al complex can independently cause vagally-mediated gastric motor excitatio
n. (C) 1999 Elsevier Science B.V. All rights reserved.