Effects of electroconvulsive therapy on striatal morphology, physiology and motor learning in a mouse model of Parkinson’s disease

≪p≫Parkinson's disease is the second most common neurodegenerative disease worldwide and currently has no causal treatment. The progressive loss of dopamine-producing neurons is not only symptomatically expressed by the cardinal motor symptoms (e.g., slowing of movement), but also causes morphological and functional changes in the postsynaptic neurons in the striatum. These changes are in turn associated with the occurrence of motor complications; normalization of striatal function could therefore be a disease-modifying approach. Against this background, electroconvulsive therapy (ECT) is a promising method because it can efficiently induce neuroplastic changes. Since its introduction in psychiatry in the 1930s, ECT has been steadily improved and is currently considered the most effective treatment for patients with treatment-resistant depression and psychosis. In the context of Parkinson's disease, ECT was shown to improve motor symptoms and fluctuations in addition to neuropsychiatric symptoms. The release of neurotrophic factors and stimulation of adult neurogenesis are discussed as mechanisms of action of ECT. Whether these factors contribute to reorganization of corticostriatal or nigrostriatal circuits, and which structural changes underlie motor improvement, is not yet known. This project therefore aims to investigate the behavioral, functional, and morphological effects of ECT in a mouse model of Parkinson's disease.≪/p≫