Electroconvulsive shock enhances striatal dopamine D1 and D3 receptor binding and improves motor performance in 6-OHDA-lesioned rats

• Published in: Journal of psychiatry & neuroscience 2007-05, Vol.32 (3), p.193-202
• Main Authors: Strome, Elissa M, Zis, Athanasios P, Doudet, Doris J
• Format: Article
• Language: English
• Subjects: Animals; Binding, Competitive; Biological and medical sciences; Corpus Striatum - metabolism; Disease Models, Animal; Electroconvulsive Therapy - methods; Fundamental and applied biological sciences. Psychology; Male; Medical Education; Medical sciences; Oxidopamine; Parkinsonian Disorders - chemically induced; Parkinsonian Disorders - therapy; Psychiatry; Psychoanalysis; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Psychomotor Performance - physiology; Psychopathology. Psychiatry; Rats; Rats, Sprague-Dawley; Receptors, Dopamine D1 - metabolism; Receptors, Dopamine D3 - metabolism; Research Paper; Sympatholytics
• ISSN: 1180-4882; 1488-2434
• DOI: 10.1016/S1180-4882(07)50030-2

Objective Electroconvulsive therapy (ECT) is a widely used and effective treatment for mood disorders and appears to have positive effects on the motor symptoms of Parkinson’s disease (PD), improving motor function for several weeks. Because repeated electroconvulsive shock (ECS) in normal animals enhances striatal dopamine (DA) D1 and D3 receptor binding, we hypothesized that upregulation of D1 and D3 receptors may also be occurring in the parkinsonian brain after repeated ECS treatment. Methods Rats were rendered hemiparkinsonian through unilateral infusion of the DA-specific neurotoxin 6-hydroxydopamine into the medial forebrain bundle and substantia nigra. The animals were tested for hindlimb and forelimb function before and 48 hours after the last of 10 daily treatments with ECS or sham. After sacrifice, DA receptor binding was determined autoradiographically. Results While there was no increase in forelimb use in the cylinder test, ECS treatment significantly improved hindlimb motor performance on a tapered beam-walking test and enhanced striatal D1 and D3 receptor binding, without affecting D2 receptor binding. Conclusion This study suggests that at least part of the mechanism of action of ECT in PD may be enhanced DA function within the direct pathway of the basal ganglia and may support the further study and use of ECT as a potential adjunct treatment for PD.