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梨状皮质中央而非前部或后部的双侧损伤会延缓大鼠杏仁核点燃。

Bilateral lesions of the central but not anterior or posterior parts of the piriform cortex retard amygdala kindling in rats.

作者信息

Schwabe K, Ebert U, Löscher W

机构信息

Department of Pharmacology, Toxicology and Pharmacy, School of Veterinary Medicine, Bünteweg 17, D-30559, Hannover, Germany.

出版信息

Neuroscience. 2000;101(3):513-21. doi: 10.1016/s0306-4522(00)00407-3.

Abstract

The piriform cortex is thought to be involved in temporal lobe seizure propagation, such as that occurring during kindling of the amygdala or hippocampus. A number of observations suggested that the circuits of the piriform cortex might act as a critical pathway for limbic seizure discharges to assess motor systems, but direct evidence for this suggestion is scarce. Furthermore, the piriform cortex is not a homogeneous structure, which complicates studies on its role in limbic epileptogenesis. We have previously reported data indicating that the central part of the piriform cortex might be particularly involved during amygdala kindling. In order to further evaluate the role of different parts of the piriform cortex during kindling development, we bilaterally destroyed either the central, anterior or posterior piriform cortex by microinjections of ibotenate two weeks before onset of amygdala kindling. Lesions of the anterior piriform cortex hardly affected kindling acquisition, except that fewer animals exhibited stage 3 (unilateral forelimb) seizures compared to sham controls. Lesions of the central piriform cortex significantly retarded kindling, which was due to a decreased progression from stage 3 to stage 4/5 seizures, i.e. the lesioned rats needed significantly longer for the acquisition of generalized clonic seizures in the late stages of kindling development. Lesions of the posterior piriform cortex did not significantly affect kindling development. The data demonstrate that different parts of the piriform cortex mediate qualitatively different effects on amygdala kindling. The central piriform cortex seems to be a neural substrate involved in the continuous development of kindling from stage 3 to stages 4/5, indicating that this part of the piriform cortex may have preferred access, either directly or indirectly, to structures capable of supporting generalized kindled seizure expression.

摘要

梨状皮质被认为参与颞叶癫痫发作的传播,比如在杏仁核或海马体点燃过程中发生的癫痫发作。多项观察结果表明,梨状皮质的神经回路可能作为边缘系统癫痫放电评估运动系统的关键通路,但这一观点的直接证据却很少。此外,梨状皮质并非均匀结构,这使得研究其在边缘系统癫痫发生中的作用变得复杂。我们之前曾报道数据表明,在杏仁核点燃过程中,梨状皮质的中央部分可能特别受累。为了进一步评估梨状皮质不同部分在点燃发展过程中的作用,我们在杏仁核点燃开始前两周,通过双侧微量注射鹅膏蕈氨酸损毁梨状皮质的中央、前部或后部。除了与假手术对照组相比,表现出3期(单侧前肢)癫痫发作的动物较少外,前部梨状皮质的损伤几乎不影响点燃的获得。中央梨状皮质的损伤显著延缓了点燃,这是由于从3期到4/5期癫痫发作的进展减少,即损伤大鼠在点燃发展后期获得全身性阵挛性癫痫发作所需的时间显著更长。后部梨状皮质的损伤对点燃发展没有显著影响。这些数据表明,梨状皮质的不同部分对杏仁核点燃介导的影响在性质上有所不同。中央梨状皮质似乎是参与从3期到4/5期点燃持续发展的神经基质,这表明梨状皮质的这一部分可能直接或间接地优先连接到能够支持全身性点燃癫痫发作表达的结构。

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