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黑质网状部神经元的激活:在点燃性癫痫发作的起始和行为表现中的作用。

Activation of substantia nigra pars reticulata neurons: role in the initiation and behavioral expression of kindled seizures.

作者信息

Bonhaus D W, Russell R D, McNamara J O

机构信息

Department of Pharmacology, Duke University Medical Center, Durham, NC.

出版信息

Brain Res. 1991 Apr 5;545(1-2):41-8. doi: 10.1016/0006-8993(91)91267-5.

Abstract

Numerous studies have implicated the substantia nigra pars reticulata (SNR) in the initiation and behavioral expression of kindled seizures. In immobilized, amygdala-kindled animals, SNR neurons have been shown to enter an intense burst-firing pattern during afterdischarge (AD). Taken together these findings raised the possibility that the SNR facilitates the expression of kindled seizures by directly propagating seizure activity into target structures. In this study we examined the relationship between activation of SNR neurons and the electrical (EEG) and behavioral (clonic motor) expression of kindled seizures using both immobilized and unrestrained animals. The principal findings were that: (1) in both immobilized and unrestrained animals the SNR neurons of kindled, but not control, animals were recruited into a burst-firing pattern during AD; (2) the onset of burst-firing was delayed until after the onset of AD; and (3) the onset of burst-firing was not correlated with the onset of rhythmic motor seizure activity. These findings support the idea that the development of kindling is associated with recruitment of SNR neurons into a seizure propagating network. However, these data suggest that activation of SNR neurons is not necessary for the expression of clonic motor activity and does not lower seizure threshold.

摘要

众多研究表明,黑质网状部(SNR)与点燃性癫痫发作的起始及行为表现有关。在固定不动的杏仁核点燃动物中,已表明SNR神经元在放电后(AD)期间会进入强烈的爆发式放电模式。综合这些发现,提出了一种可能性,即SNR通过将癫痫活动直接传播到目标结构来促进点燃性癫痫发作的表达。在本研究中,我们使用固定不动和不受约束的动物,研究了SNR神经元的激活与点燃性癫痫发作的电活动(脑电图,EEG)和行为表现(阵挛性运动)之间的关系。主要发现如下:(1)在固定不动和不受约束的动物中,点燃动物而非对照动物的SNR神经元在AD期间被募集到爆发式放电模式;(2)爆发式放电的起始延迟至AD起始之后;(3)爆发式放电的起始与节律性运动癫痫活动的起始不相关。这些发现支持了这样一种观点,即点燃的发展与SNR神经元被募集到癫痫传播网络有关。然而,这些数据表明,SNR神经元的激活对于阵挛性运动活动的表达不是必需的,并且不会降低癫痫阈值。

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