Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 42, Pages 14182-14193Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2149-10.2010
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Funding
- European Community [222918]
- cPADS Grant [217902]
- Progetto Strategico
- Progetti Finalizzati Multicentrici Programma Neuroscienze Compagnia di San Paolo
- Progetto Ministero della Salute
- Young Italian Researchers Grants
- Fondation de la Recherce Medicale
- Progetti Finalizzati
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A correct interplay between dopamine (DA) and glutamate is essential for corticostriatal synaptic plasticity and motor activity. In an experimental model of Parkinson's disease (PD) obtained in rats, the complete depletion of striatal DA, mimicking advanced stages of the disease, results in the loss of both forms of striatal plasticity: long-term potentiation (LTP) and long-term depression (LTD). However, early PD stages are characterized by an incomplete reduction in striatal DA levels. The mechanism by which this incomplete reduction in DA level affects striatal synaptic plasticity and glutamatergic synapses is unknown. Here we present a model of early PD in which a partial denervation, causing mild motor deficits, selectively affects NMDA-dependent LTP but not LTD and dramatically alters NMDA receptor composition in the postsynaptic density. Our findings show that DA decrease influences corticostriatal synaptic plasticity depending on the level of depletion. The use of the TAT2A cell-permeable peptide, as an innovative therapeutic strategy in early PD, rescues physiological NMDA receptor composition, synaptic plasticity, and motor behavior.
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