期刊
NATURE NEUROSCIENCE
卷 19, 期 7, 页码 868-875出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.4306
关键词
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资金
- Progetto di Ricerca di Interesse Nazionale (PRIN) [2010AHHP5H]
- Fondazione Cariplo [2014-0660]
- Italian Ministry of Education, University and Research
- FIRE Call Program Futuro in Ricerca [RBFR13S4LE_002]
- Italian Ministry of Health
- Ricerca Finalizzata
- Giovani Ricercatori [GR-2010-2316671, RF-2013-02357386, RF-2013-02356215]
Recent clinical and preclinical studies have shown that hyperkinetic disorders such as Huntington's disease, dystonia and L-DOPA-induced dyskinesia in Parkinson's disease are all characterized by loss of the ability to reverse synaptic plasticity and an associated increase in the excitability of excitatory neuronal inputs to a range of cortical and subcortical brain areas. Moreover, these changes have been detected in humans with hyperkinetic disorders either via direct recordings from implanted deep brain electrodes or noninvasively using transcranial magnetic stimulation. Here we discuss the mechanisms underlying the loss of bidirectional plasticity and the possibility that future interventions could be devised to reverse these changes in patients with hyperkinetic movement disorders.
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