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Protection of dopaminergic neurons by electroconvulsive shock in an animal model of Parkinson’s disease
Author(s) -
Anastasia Agustín,
De Erausquin Gabriel A.,
Wojnacki José,
Mascó Daniel H.
Publication year - 2007
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.04856.x
Subject(s) - glial cell line derived neurotrophic factor , dopaminergic , neuroprotection , substantia nigra , neurotrophic factors , oxidopamine , parkinson's disease , dopamine , neuroscience , medicine , pharmacology , endocrinology , chemistry , biology , receptor , disease
Electroconvulsive shock (ECS) improves motor function in Parkinson’s disease. In rats, ECS stimulates the expression of various factors some of which have been proposed to exert neuroprotective actions. We have investigated the effects of ECS on 6‐hydroxydopamine (6‐OHDA)‐injected rats. Three weeks after a unilateral administration of 6‐OHDA, 85–95% nigral dopaminergic neurons are lost. Chronic ECS prevented this cell loss, protect the nigrostriatal pathway (assessed by FloroGold retrograde labeling) and reduce motor impairment in 6‐OHDA‐treated animals. Injection of 6‐OHDA caused loss of expression of glial cell‐line derived neurotrophic factor (GDNF) in the substantia nigra. Chronic ECS completely prevented this loss of GDNF expression in 6‐OHDA‐treated animals. We also found that protected dopaminergic neurons co‐express GDNF receptor proteins. These results strongly suggest that endogenous changes in GDNF expression may participate in the neuroprotective mechanism of ECS against 6‐OHDA induced toxicity.