Hyperkinetic disorders and loss of synaptic downscaling
Hyperkinetic disorders and loss of synaptic downscaling
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DOI：
10.1038/nn.4306
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发表时间：
2016-07-01
影响因子：
25
通讯作者：
Picconi, Barbara
中科院分区：
文献类型：
--
作者：
Calabresi, Paolo;Pisani, Antonio;Picconi, Barbara
最近的临床和临床前研究已经表明，运动过度障碍例如亨廷顿病、帕金森病中的肌张力障碍和L-DOPA诱导的运动障碍的特征都在于逆转突触可塑性的能力的丧失和对一系列皮层和皮层下脑区域的兴奋性神经元输入的兴奋性的相关增加。此外，这些变化已经在患有多动障碍的人类中通过植入脑深部电极的直接记录或使用经颅磁刺激的非侵入性检测到。在这里，我们讨论了双向可塑性丧失的潜在机制，以及未来的干预措施可以逆转多动症患者的这些变化。
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.