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首页> 外文期刊>The European Journal of Neuroscience >Subregional changes in discharge rate, pattern, and drug sensitivity of putative GABAergic nigral neurons in the kindling model of epilepsy.
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Subregional changes in discharge rate, pattern, and drug sensitivity of putative GABAergic nigral neurons in the kindling model of epilepsy.

机译：癫痫点燃模型中假定的GABA能神经向神经元放电速率，模式和药物敏感性的亚区域变化。

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The substantia nigra pars reticulata (SNr) is thought to act as a seizure-gating mechanism in kindling and other epilepsy models. We investigated whether the kindling process induces site-specific (anterior-posterior) and seizure-outlasting alterations in the activity of putative GABAergic SNr neurons and in their response to pharmacological manipulation. Female Wistar rats were kindled via the basolateral amygdala by daily stimulation. In vivo extracellular single unit recordings of SNr neurons were performed in kindled rats 1 day after a generalized seizure in order to examine activity changes that outlast the kindled seizures. Sham-kindled and naive rats served as controls. We found a significant and seizure-outlasting increase of discharge rates within the posterior but not within the anterior SNr of kindled rats when compared to controls. Furthermore, kindling resulted in seizure-outlasting burst-like firing pattern of SNr neurons. The antiepileptic drug valproic acid (VPA; 100 mg/kg i.v.) significantly reduced SNr discharge rates in all animal groups. Interestingly, neurons located in the anterior SNr of kindled rats were significantly less depressed by VPA compared to the reduction obtained in naive controls. The present data disclose kindling induced functional plasticity within basal ganglia regions. The findings are relevant for a better understanding of the mechanisms underlying the seizure-gating function of the SNr and might provide new targets for rational therapeutic manipulations, which aim to establish a remote control of epileptic seizures.
机译：黑质网状黑质（SNr）被认为在点燃和其他癫痫模型中起癫痫发作的控制机制。我们调查了点燃过程是否在假定的GABA能SNr神经元的活性及其对药理反应的反应中诱导了特定部位（前后）和癫痫发作持续性改变。每天刺激通过基底外侧杏仁核点燃雌性Wistar大鼠。全身性癫痫发作1天后，在点燃的大鼠中进行SNr神经元的体内细胞外单个单位录音，以检查比点燃的癫痫发作更持久的活性变化。假种和幼稚大鼠作为对照。我们发现，与对照组相比，点燃的大鼠后部而不是前部SNr内放电率显着增加且癫痫持续持续增加。此外，点燃会导致SNr神经元的癫痫发作持续发作。抗癫痫药丙戊酸（VPA; 100 mg / kg腹腔注射）显着降低了所有动物组的SNr释放率。有趣的是，与幼稚对照组相比，被点燃的大鼠前SNr中的神经元受VPA的抑制作用明显降低。本数据公开了点燃引起的基底神经节区域内的功能可塑性。这些发现与更好地了解SNr的癫痫发作门控功能的机制有关，并且可能为合理的治疗操作提供新的目标，旨在建立对癫痫发作的远程控制。

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