Antiparkinsonian mechanism of electroconvulsive therapy in MPTP-lesioned non-human primates

Electroconvulsive therapy (ECT), an effective treatment for depression, also improves motor symptomatology in Parkinson's disease (PD). We have previously demonstrated that ECT stimulates dopamine (DA) function in the striatum of healthy non-human primates, suggesting that DA may contribute to antidepressant effects.

We investigated the potential role of DA mechanisms in the amelioration of PD symptoms following a clinical course of ECT.

We treated non-human primates rendered mildly bilaterally or unilaterally parkinsonian with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), with a course of 6 ECT treatments. Using positron emission tomography, animals were scanned at baseline and at various time points after ECT with tracers of the DA system. Data were analyzed using the Logan reference tissue model and statistics were performed using orthogonal polynomial contrasts.

There was no change in binding of the DA transporter tracer in the lesioned striata after ECT as opposed to what we measured in the striatum of healthy animals. Raclopride binding to the D(2/3) receptors was unaffected in all groups. However, there were increases in vesicular monoamine transporter type 2 and D(1) receptor binding in the MPTP-lesioned striata after ECT, returning towards baseline by 6 weeks.

We suggest that the effects of ECT in PD may proceed from a mechanism similar to that in healthy animals but with a blunted dopaminergic response, likely due to the significant loss of striatal DA terminals. The safety of ECT, its mild side effects and its stimulatory effects of the DA system may thus make it an attractive adjunct to antiparkinsonian treatment.