Effects of drug manipulations on anterior components of somatosensory evoked potentials in a parkinsonian animal model.

Somatosensory Evoked Potentials (SEPs) to median nerve stimuli were recorded in seven Cynomolgus monkeys before and after the induction of the MPTP-parkinsonian syndrome. SEPs recorded after the onset of parkinsonism showed a significant amplitude reduction of an anterior negative component peaking at about 15 ms (N15), independent of the severity of symptoms. The amplitude decrease was not reversed by the administration of I-dopa, despite clinical improvement, or cholinergic, noradrenergic and gabaergic agents. Amplitudes of N15 and of parietal P15 components were increased by the administration of the N-MDA antagonists ketamine and MK 801, and markedly increased when monkeys were given the anaesthetic agent etomidate. The present study shows that the reduced N15 SEP component of parkinsonian monkeys is similar to the reduced frontal N30 SEP component evidenced by other authors in patients affected by Parkinson's disease. The attenuation of N15 is not related to deficitary dopaminergic, noradrenergic, cholinergic and gabaergic systems. The implications of this finding and the role of glutamate toxicity are discussed.