Abstract
Three excitatory amino acid agonists [N-methyl-D-aspartate (NMDA), kainate and alpha-amino-2,3-dihyro-5-methyl-3-oxo-4-isoxalzolepropanoic acid], each selective for separate glutamate binding sites, were evaluated for dipsogenic responses in pigeons. NMDA and kainate produced a reliable and rapid drinking response (up to 30% of body weight over 3 hr). alpha-amino-2,3-dihyro-5-methyl-3-oxo-4-isoxalzolepropanoic acid, up to doses which produced profound effects on motor behavior (18.0 mg/kg i.m.), did not produce a reliable drinking response. The dipsogenic effects of NMDA and its stereoisomer, N-methyl-L-aspartate, were antagonized by the competitive NMDA antagonist, cis-4-(phosphonomethyl)-2-piperidinecarboxylic acid. cis-4-(phosphonomethyl)-2-Piperidinecarboxylic acid failed to prevent drinking produced by kainate or water deprivation. These results suggest that NMDA-, kainate- and water deprivation-induced drinking are mediated via separate mechanisms and that NMDA induced drinking is mediated via NMDA receptors.
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