Vagally-regulated gastric motor activity: evidence for kainate and NMDA receptor mediation

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.