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杏仁核损伤会增加大鼠海马内注射 kainic 酸的毒性,并减少自发性复发性癫痫的后期发作。

Amygdaloid lesion increases the toxicity of intrahippocampal kainic acid injection and reduces the late occurrence of spontaneous recurrent seizures in rats.

作者信息

Cavalheiro E A, Calderazzo Filho L S, Riche D, Feldblum S, Le Gal la Salle G

出版信息

Brain Res. 1983 Mar 7;262(2):201-7. doi: 10.1016/0006-8993(83)91009-0.

Abstract

Spontaneous recurrent seizures (SRS) following intrahippocampal kainic acid (KA) injection have been described in a previous paper from our laboratory. The SRSs are clinically similar to the seizures induced by kindling the amygdala and we suggested that the amygdala plays a role in initiating the SRSs. Accordingly, the present paper examines the effect of amygdaloid lesions on intrahippocampal KA-treated rats. There were short- and long-term effects. (1) Short-term: the toxicity of KA was increased in lesioned animals. Status epilepticus followed by death of the animals was evoked with half of the dose required to cause the same effect in intact rats. Moreover, a gross haematuria was encountered 6-12 h after KA injection. This was not observed in non-lesioned rats even following the highest KA doses. (2) Long-term: amygdaloid lesions delayed the occurrence of the SRSs, reduced their incidence and modified their expression. In lesioned animals seizures began with a period of tonic immobility with no sign of the masticatory movements seen in intact animals. Histological examination of the KA-induced lesions did not show any major differences between lesioned and intact animals. It is suggested that the short-term effects are due to an unspecific effect on homeostatic mechanisms, whereas the long-term ones reflect a specific involvement of the amygdala in the late appearing seizures.

摘要

我们实验室之前的一篇论文描述了海马内注射红藻氨酸(KA)后出现的自发性反复癫痫发作(SRS)。这些SRS在临床上与杏仁核点燃诱发的癫痫发作相似,我们认为杏仁核在引发SRS中起作用。因此,本文研究了杏仁核损伤对海马内注射KA处理的大鼠的影响。存在短期和长期影响。(1)短期:损伤动物中KA的毒性增加。用在完整大鼠中产生相同效果所需剂量的一半即可诱发癫痫持续状态,随后动物死亡。此外,KA注射后6 - 12小时出现明显血尿。即使给予最高剂量的KA,在未损伤的大鼠中也未观察到这种情况。(2)长期:杏仁核损伤延迟了SRS的发生,降低了其发生率并改变了其表现形式。在损伤动物中,癫痫发作开始时会有一段强直性不动期,没有完整动物中出现的咀嚼运动迹象。对KA诱导损伤的组织学检查显示,损伤动物和完整动物之间没有任何主要差异。提示短期影响是由于对稳态机制的非特异性作用,而长期影响则反映了杏仁核在后期出现的癫痫发作中的特异性参与。

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