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Brain Advance Access originally published online on January 22, 2009
Brain 2009 132(2):285-287; doi:10.1093/brain/awn340
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© The Author (2009). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Scientific Commentary

Synaptic plasticity, dopamine and Parkinson's disease: one step ahead

Paolo Calabresi1,2, Nicola Biagio Mercuri2,3 and Massimiliano Di Filippo1,2

1Clinica Neurologica, Università di Perugia, Perugia, Italy 2IRCCS Fondazione S. Lucia, Rome, Italy 3Clinica Neurologica, Università di Roma Tor Vergata, Rome, Italy

Email:calabre@unipg.it

The first 150 words of the full text of this article appear below.

The progressive loss of substantia nigra pars compacta neurons that characterizes Parkinson's disease pathology leads to impaired levels of dopamine in several key structures of the basal ganglia neuronal circuit and subsequent alteration of the thinly regulated balance between activities of the output nuclei—the internal segment of the globus pallidus and the substantia nigra pars reticulata—that is considered essential for normal function of the circuit (Fig. 1A).


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  		Fig. 1 The basal ganglia circuit. Potential implications of the LTP of GABAergic signals onto substantia nigra pars reticulata neurons. (a) During physiological conditions the thinly regulated activity of the direct and indirect pathways controls the activity of the output nuclei. (b) During Parkinson's disease, in the absence of a pharmacological treatment, dopamine deficiency causes overactivity of the indirect pathway and reduced activity of the inhibitory GABAergic direct pathway, disinhibiting the output nuclei and thus causing excessive inhibition of . . . [Full Text of this Article]

 

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