The involvement of N-methyl-D-aspartate receptors in plasticity induced by paired corticospinal-motoneuronal stimulation in humans

Plasticity can be induced at human corticospinal-motoneuronal synapses by delivering repeated, paired stimuli to corticospinal axons and motoneurones in a technique called paired corticospinal-motoneuronal stimulation (PCMS). To date, the mechanisms of the induced plasticity are unknown. To determine whether PCMS-induced plasticity is dependent on N-methyl-D-aspartate receptors (NMDARs), the effect of the non-competitive NMDAR antagonist, dextromethorphan, on PCMS-induced facilitation was assessed in a two-day, double-blind, placebo-controlled experiment. PCMS consisted of 100 pairs of stimuli, delivered at an interstimulus interval that produces facilitation at corticospinal-motoneuronal synapses that excite biceps brachii motoneurones. Transcranial magnetic stimulation (TMS) elicited corticospinal volleys, which were timed to arrive at corticospinal-motoneuronal synapses just prior to antidromic potentials elicited in motoneurones using electrical brachial plexus stimulation. To measure changes in the corticospinal pathway at a spinal level, biceps responses to cervicomedullary stimulation (cervicomedullary motor evoked potentials, CMEPs) were measured before and for 30 min after PCMS. Individuals who displayed a ≥10% increase in CMEP size after PCMS on screening were eligible to take part in the two-day experiment. Following PCMS, there was a significant difference in CMEP area between placebo and dextromethorphan days (p=0.014). On the placebo day, PCMS increased average CMEP areas to 127±46% of baseline, whereas on the dextromethorphan day, CMEP area was decreased to 86±33% of baseline (mean±SD; placebo: n=11; dextromethorphan: n=10). Therefore, dextromethorphan suppressed the facilitation of CMEPs after PCMS. This indicates that plasticity induced at synapses in the human spinal cord by PCMS may be dependent on NMDARs.

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