A potassium channel blocker induces a long-lasting enhancement of corticostriatal responses.
A potassium channel blocker induces a long-lasting enhancement of corticostriatal responses.
复制标题
钾通道阻滞剂可诱导皮质纹状体反应的持久增强。
DOI：
10.1016/j.neuropharm.2004.09.018
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Winder,DannyG
中科院分区：
文献类型：
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作者：
Norman,EricD;Egli,RegulaE;Colbran,RogerJ;Winder,DannyG
背纹状体突触可塑性的破坏可能有助于帕金森病的病理生理基础。在这里，我们报告了一种新的化学诱导的可塑性形式，由钾通道阻滞剂四乙基铵（TEA）在成年大鼠背外侧纹状体中的应用诱导。短暂应用TEA持续增加突触诱发的细胞外记录皮质纹状体反应，以活动、浓度和时间依赖的方式。药理实验表明，这种可塑性依赖于l型钙通道和蛋白激酶C （PKC）的激活。6-羟多巴胺显著降低了黑质纹状体多巴胺损伤引起的纹状体多巴胺消耗，但没有消除tea介导的皮质纹状体反应增强。细胞内记录表明，这种由tea介导的可塑性与EPSP大小和坡度的增加以及输入电阻有关。总的来说，这些发现证明了在缺乏多巴胺能输入的情况下，成人背纹状体中l型钙通道依赖性可塑性的一种新形式。
Disruptions in synaptic plasticity in the dorsal striatum may contribute to the pathophysiology underlying Parkinson's disease. Here we report a novel, chemically-induced form of plasticity induced by application of the potassium channel blocker tetraethylammonium (TEA) in the dorsolateral striatum of the adult rat. Transient application of TEA persistently increased synaptically-evoked extracellularly-recorded corticostriatal responses in an activity-, concentration- and time-dependent manner. Pharmacological experiments suggest that this plasticity is dependent on L-type calcium channel and protein kinase C (PKC) activation. Striatal dopamine depletion induced by nigrostriatal dopamine lesions with 6-hydroxydopamine significantly reduced, but did not abolish, TEA-mediated enhancement of the corticostriatal response. Intracellular recordings demonstrate that this TEA-mediated plasticity is associated with an increase in EPSP size and slope, as well as input resistance. Collectively, these findings demonstrate a novel form of L-type calcium channel-dependent plasticity in the adult dorsal striatum that is induced in the absence of dopaminergic input.