title: Electroconvulsive shock enhances striatal dopamine D1 and D3 receptor binding and improves motor performance in 6-OHDA-lesioned rats.
abstract: 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) D(1) and D(3) receptor binding, we hypothesized that upregulation of D(1) and D(3) receptors may also be occurring in the parkinsonian brain after repeated ECS treatment.
  
  
  METHODS
  Rats were rendered hemi-parkinsonian 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 D(1) and D(3) receptor binding, without affecting D(2) receptor binding.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, BC. strome@interchange.ubc.ca
authors.forename: Elissa M
authors.initials: EM
authors.lastname: Strome
authors.forename: Athanasios P
authors.initials: AP
authors.lastname: Zis
authors.forename: Doris J
authors.initials: DJ
authors.lastname: Doudet
mesh_terms: D000818:Animals; D001667:Binding, Competitive; D003342:Corpus Striatum / Q000378:metabolism*; D004195:Disease Models, Animal; D004565:Electroconvulsive Therapy / Q000379:methods*; D008297:Male; D016627:Oxidopamine; D020734:Parkinsonian Disorders / Q000139:chemically induced / Q000628:therapy*; D011597:Psychomotor Performance / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017447:Receptors, Dopamine D1 / Q000378:metabolism*; D050637:Receptors, Dopamine D3 / Q000378:metabolism*; D013565:Sympatholytics
chemical_list: D017447:Receptors, Dopamine D1; D050637:Receptors, Dopamine D3; D013565:Sympatholytics; D016627:Oxidopamine