Intrathecally administered N-methyl-D-aspartate increases persistent hindlimb flexion in rat

Persistent hindlimb flexion was induced in pentobarbital anesthetized rats using a prolonged, electrical stimulus. Intrathecal (i.t.) N-methyl-D-aspartate NMDA) (1 mM, 5 microliters) applied prior to stimulation increased flexion relative to stimulated controls subsequent to stimulation (156%); 3 days later (109%) and after spinalization at 3 days (91%). Pretreatment with MK-801 (3 mg/kg, i.p.) prevented the enhancement of flexion. Withdrawal latencies to a thermal stimulus also were measured. I.t. NMDA plus stimulation reduced mean latency relative to controls only subsequent to stimulation. Latencies were increased by MK-801 post-injection, post-stimulation and at 3 days. The results suggest that the induction of persistent hindlimb flexion depends upon spinal NMDA receptors.