Endogenous morphine-like compound immunoreactivity increases in parkinsonism.
Brain. 2011-07-08; 134(8): 2321-2338
DOI: 10.1093/brain/awr166
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1. Brain. 2011 Aug;134(Pt 8):2321-38. doi: 10.1093/brain/awr166. Epub 2011 Jul 8.
Endogenous morphine-like compound immunoreactivity increases in parkinsonism.
Charron G(1), 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.
Author information:
(1)University of Bordeaux, Institut des Maladies Neurodegeneratives, Bordeaux,
France.
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.
DOI: 10.1093/brain/awr166
PMID: 21742735 [Indexed for MEDLINE]