TACHYCARDIA AFTER GLUTAMATE INJECTION IN RAT SPINAL-CORD IS NOT BLOCKED BY KYNURENATE OR MIMICKED BY METABOTROPIC AGONISTS

1. We have used microinjections of glutamate, an ionotropic excitatory amino acid receptor antagonist (kynurenate) and selective ionotropic (NMDA and kainate) and metabotropic (1S-3R-ACPD, trans-ACPD and L-AP4) receptor agonists in the thoracic IML of the rat to define the recept ors mediating the tachycardia produced by excitatory amino acid agonis ts. 2. Injection of glutamate (Delta heart rate = 76 +/- 8 beats/min n = 16), NMDA (Delta heart rate = 116.5 +/- 5 beats/min n = 6) or kaina te (Delta heart rate = 92 +/- 22 beats/min n = 6) evokes a tachycardia when injected into the thoracic intermediolateral column. Kynurenate blocked the response to NMDA(-2% of initial response) and markedly att enuated the response to kainate (14% of initial response) but did mot alter the response to glutamate (106% of initial response), 3. IS-3R-A CPD did not elicit a tachycardia when injected into the thoracic inter mediolateral column and neither trans-ACPD nor L-AP4 induced a tachyca rdia after kynurenate injection into the thoracic intermediolateral co lumn. 4. Thus stimulation of either NMDA or AMPA/kainate receptors eli cits a tachycardia in rat thoracic spinal cord but glutamate also acti vates another receptor type to elicit a tachycardia. The lack of a tac hycardia when trans-ACPD, 1S-3R-ACPD or L-AP4 were injected into the t horacic spinal cord suggests that the kynurenate resistant tachycardia elicited by glutamate is not mediated by metabotropic receptors. The kynurenate resistant tachycardia elicited by glutamate is not mediated by any of the known excitatory amino acid receptor types.