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丘脑前核高频电刺激对大鼠的抗惊厥作用。

Anticonvulsant effect of anterior thalamic high frequency electrical stimulation in the rat.

作者信息

Mirski M A, Rossell L A, Terry J B, Fisher R S

机构信息

Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

出版信息

Epilepsy Res. 1997 Sep;28(2):89-100. doi: 10.1016/s0920-1211(97)00034-x.

DOI:10.1016/s0920-1211(97)00034-x
PMID:9267773
Abstract

Evidence suggests that a specific subcortical pathway synaptically linking the anterior thalamic nuclear complex (AN) to the hypothalamus and midbrain is important in the expression of pentylenetetrazol (PTZ) seizures. Perturbation of neuronal activity along this path via focal disruption or chemical inhibition significantly raises seizure threshold. Recent data has demonstrated that focal electrical stimulation within the hypothalamic component of this pathway inhibited seizure expression in a current and frequency dependent fashion. Similar experiments were conducted in the AN to investigate the hypothesis that stimulation of this thalamic nuclear region can prevent the propagation of PTZ seizures between cortical and subcortical regions. Our results indicate that high frequency (100 Hz) stimulation of AN did not alter the expression of low dose PTZ induced cortical bursting but did raise the clonic seizure threshold compared to naive animals or those stimulated at sites near, but not in AN (P < 0.01). Low frequency stimulation (8 Hz) was in contrast, proconvulsant and could induce behavioral arrest responses accompanied by rhythmic high voltage EEG even without PTZ challenge. This data further highlights the role of AN in mediating the expression of seizures and provides experimental support for the concept that this thalamic region may be a promising target for focal stimulation to treat intractable seizures in humans.

摘要

有证据表明,一条将丘脑前核复合体(AN)与下丘脑和中脑通过突触连接起来的特定皮质下通路,在戊四氮(PTZ)诱发癫痫发作的表达中起重要作用。沿此通路的神经元活动通过局灶性破坏或化学抑制受到干扰后,癫痫发作阈值会显著提高。最近的数据表明,在该通路的下丘脑部分进行局灶性电刺激,会以电流和频率依赖的方式抑制癫痫发作的表达。在丘脑前核复合体中进行了类似实验,以研究刺激该丘脑核区域能否阻止PTZ诱发的癫痫发作在皮质和皮质下区域之间传播这一假设。我们的结果表明,与未处理的动物或在靠近但不在丘脑前核复合体部位接受刺激的动物相比,高频(100Hz)刺激丘脑前核复合体不会改变低剂量PTZ诱发的皮质爆发性活动的表达,但会提高阵挛性癫痫发作阈值(P<0.01)。相比之下,低频刺激(8Hz)具有促惊厥作用,即使在没有PTZ激发的情况下,也能诱发伴有节律性高电压脑电图的行为停止反应。这些数据进一步突出了丘脑前核复合体在介导癫痫发作表达中的作用,并为这一丘脑区域可能成为治疗人类难治性癫痫的局灶性刺激的有前景靶点这一概念提供了实验支持。

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