Application of a GABAA (gamma-aminobutyric acid-A) receptor antagonist through a microdialysis probe into the forelimb primary motor cortex of ketamine-anesthetized rats induced electromyographic activity in the contralateral forelimb. This activity consisted of spontaneous forelimb movements with a frequency of 0.8 +/- 0.2 Hz. The motor activity induced by GABAA receptor blockade was suppressed by application through the dialysis probe of a non-NMDA (N-methyl-D-aspartate) receptor antagonist, but not by an NMDA receptor antagonist. Glutamate eliminated the blocking effect of the non-NMDA receptor antagonist upon GABAA receptor blockade mediated activity. In conclusion, the results show that an excitatory input to the motor cortical output is mediated through a non-NMDA receptor, therefore the effects of cortical disinhibition may be controlled by non-NMDA receptors.