NMDA receptors in the intermediolateral column of the spinal cord mediate sympathoexcitatory cardiac responses elicited from the ventrolateral medullary pressor area.

Microinjections of L-glutamate into the intermediolateral column of the spinal cord (IML) at T1-T3 produced increases in heart rate (predominantly from the right IML) and myocardial contractility (predominantly from the left IML). Maximum responses were elicited from T2 segment. At this site, microinjections of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA), quisqualic acid, kainic acid and N-methyl-D-aspartic acid (NMDA) produced dose-dependent increases in heart rate and contractility which were blocked by kynurenate (a non-selective excitatory amino acid receptor antagonist). D-2-Aminophosphonoheptanoate (DAP-7) blocked the effects of NMDA but not kainic acid, quisqualic acid and AMPA. Bilateral microinjections of kynurenate (2 nmol) and DAP-7 (5 nmol) into the IML at T1-T3 significantly decreased the baseline values for contractility index and blocked the usual increase in contractility induced by unilateral microinjections of L-glutamate (1.77 nmol) into the ventrolateral medullary pressor area (VLPA). These observations suggest that: (1) a tonic excitatory input, involving an NMDA-like amino acid as a transmitter, is present in the IML at T1-T3 and (2) the stimulation of VLPA neurons results in the release of an NMDA-like excitatory amino acid in the IML at this level.