Endogenous morphine-like compound immunoreactivity increases in parkinsonism.
Fiche publication
Date publication
août 2011
Auteurs
Membres identifiés du Cancéropôle Est :
Dr VAN DORSSELAER Alain, Dr GOUMON Yannick
Tous les auteurs :
Charron G, Doudnikoff E, Laux A, Berthet A, Porras G, Canron MH, Barroso-Chinea P, Li Q, Qin C, Nosten-Bertrand M, Giros B, Delalande F, Van Dorsselaer A, Vital A, Goumon Y, Bezard E
Lien Pubmed
Résumé
Morphine is endogenously synthesized in the central nervous system and endogenous dopamine is thought to be necessary for endogenous morphine formation. As Parkinson's disease results from the loss of dopamine and is associated with central pain, we considered how endogenous morphine is regulated in the untreated and l-DOPA-treated parkinsonian brain. However, as the cellular origin and overall distribution of endogenous morphine remains obscure in the pathological adult brain, we first characterized the distribution of endogenous morphine-like compound immunoreactive cells in the rat striatum. We then studied changes in the endogenous morphine-like compound immunoreactivity of medium spiny neurons in normal, Parkinson's disease-like and l-DOPA-treated Parkinson's disease-like conditions in experimental (rat and monkey) and human Parkinson's disease. Our results reveal an unexpected dramatic upregulation of neuronal endogenous morphine-like compound immunoreactivity and levels in experimental and human Parkinson's disease, only partially normalized by l-DOPA treatment. Our data suggest that endogenous morphine formation is more complex than originally proposed and that the parkinsonian brain experiences a dramatic upregulation of endogenous morphine immunoreactivity. The functional consequences of such endogenous morphine upregulation are as yet unknown, but based upon the current knowledge of morphine signalling, we hypothesize that it is involved in fatigue, depression and pain symptoms experienced by patients with Parkinson's disease.
Référence
Brain. 2011 Aug;134(Pt 8):2321-38