Strychnine- and bicuculline-induced changes in the firing pattern of motoneurones during in vitro fictive locomotion reveal a possible N-methyl-D-aspartic acid (NMDA)-mediated suppression of motor discharge in wallaby (Macropus eugenii) pouch young.

Inhibitory pathways in the spinal cord play an important role in establishing the pattern of motor discharge. In the wallaby spinal cord preparation, disruption of glycinergic and gamma-amino butyric acid (GABA)ergic neurotransmission abolished the alternation between antagonistic motor pools during fictive locomotion. A new pattern of motor discharge also appeared when both glycine and GABA(A) receptors were blocked simultaneously. This discharge pattern was biphasic, characterized by a distinct pause between two bursts of motoneurone firing during each cycle of motor activity. Whole cell patch recordings showed that the second burst of motor discharge was not caused by a separate inward current at a delayed time course. Furthermore, local injection of an N-methyl-D-aspartic acid (NMDA) specific antagonist converted the biphasic discharge to a continuous burst pattern. The result suggests an NMDA-mediated mechanism, which causes a suppression of motoneurone firing when glutamate release from interneurones is enhanced in the absence of glycinergic and GABAergic inhibition.