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首页> 外文期刊>The European Journal of Neuroscience >Slow oscillatory activity of rat globus pallidus neurons in vitro.
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Slow oscillatory activity of rat globus pallidus neurons in vitro.

机译：大鼠苍白球神经元的体外缓慢振荡活动。

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The neurons in the external segment of the pallidum in the primate develop a characteristic firing pattern consisting of alternately occurring long, 2-20 s, strongly active phases and long completely silent phases when the subthalamo-pallidal excitatory inputs are blocked. The induction of the activity might be a factor in the development of dyskinesias after the loss of subthalamic output. In this study, we used globus pallidus (GPe) slice preparations obtained from juvenile rats to examined the conditions that support the alternatively occurring long depolarized and hyperpolarized phases which we refer to as the slow oscillation (SO). SO was not induced by the blockade of glutamatergic inputs but was induced by treatments that depolarized dendrites and, at the same time, hyperpolarized the somata with current injections. The treatments included elevation of extracellular K(+), application of K-current blockers and the lowering of extracellular Ca(2+). Application of TTX or intracellular BAPTA injection blocked the SO, while the SO could be maintained in hyperpolarization-activated inward current blockers, organic Ca-current blockers and up to 200 microm CdCl(2). These results suggest that Na currents play a major role in the generation of SO in vitro. It can be speculated that Na currents are involved in the development of active phases observed in the GPe after blockade of the glutamatergic inputs in vivo and that the unique property of GPe neurons in maintaining strong activity after the elimination of the glutamatergic driving force contributes to the development of motor disorders such as dyskinesia.
机译：灵长类动物苍白球外部部分的神经元发展出一种特征性的放电模式，当丘脑下-苍白球兴奋性输入受阻时，由交替出现的2-20 s长时间，强活性期和完全沉默期组成。活性的诱导可能是丘脑下输出减少后运动障碍发展的一个因素。在这项研究中，我们使用了从幼年大鼠获得的苍白球（GPe）切片制剂，研究了支持交替出现的长去极化和超极化阶段的条件，我们将其称为慢振荡（SO）。 SO不是由谷氨酸能输入的阻断诱导的，而是由使树突去极化并且同时通过当前注射使躯体超极化的治疗诱导的。治疗包括细胞外K（+）升高，钾电流阻滞剂的应用和细胞外Ca（2+）的降低。 TTX或细胞内BAPTA注射的应用阻止了SO，而SO可以保持在超极化激活的内向电流阻滞剂，有机Ca电流阻滞剂和高达200微米的CdCl（2）中。这些结果表明，钠电流在体外产生SO中起主要作用。可以推测，在体内阻断谷氨酸能输入后，Na电流参与了GPe中观察到的活性期的发展，并且在消除了谷氨酸能驱动力后，GPe神经元在维持强活性方面的独特性质有助于神经元的发育。运动障碍如运动障碍的发展。

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