The effects of electroconvulsive shock on dopamine-1 and dopamine-2 receptor ligand binding activity in MPTP-treated mice

To explore the possible therapeutic use of electric convulsive treatment in Parkinson's disease (PD), the authors examined the biochemical effects of electroconvulsive shock (ECS) on dopaminergic systems in a rodent model of PD, induced with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). MPTP increased dopamine turnover, as indicated by an increase in the ratio of the dopamine metabolites dihydroxyphenylacetic acid and homovanillic acid to dopamine. [³H]Spiperone binding to the D₂ site increased after lesioning of striatal dopamine terminals. With ECS alone, no changes were found in monoamine levels, brain monoamine oxidase activity, or the D₂-labeled sites measured 24 hours after the last treatment. [³H]SCH-23390 binding to the D₁ site increased after ECS. In MPTP-treated mice, ECS also increased [³H]SCH-23390 binding to the D₁ site, whereas [³H]spiperone binding to the D₂ site was unchanged compared to control or to only ECS-treated animals, and decreased compared to the MPTP-treated group that did not receive ECS. ECS appears to selectively modify both the D₁ and D₂ sites when given after MPTP, increasing the binding of a D₁ radioligand and decreasing the binding of a D₂ radioligand.