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在大鼠梨状皮质中央进行双侧微注射氨己烯酸可延缓杏仁核点燃。

Bilateral microinjections of vigabatrin in the central 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, University of Veterinary Medicine Hannover, Bünteweg 17, D-30559 Hannover, Germany.

出版信息

Neuroscience. 2004;129(2):425-9. doi: 10.1016/j.neuroscience.2004.08.013.

Abstract

The piriform cortex (PC) is the largest region of the mammalian olfactory cortex with strong connections to limbic structures, including the amygdala, hippocampus, and entorhinal cortex. Various previous studies in rodents suggest that the PC might be very important in the development and maintenance of limbic kindling, i.e. a widely used model of temporal lobe epilepsy. GABAergic inhibition in the transition zone between the anterior and posterior PC, termed here central PC, seems to be particularly involved in the processes leading to progression of kindled seizures. This prompted us to study whether elevation of GABA levels in this subregion of the PC by bilateral microinjection of vigabatrin is capable of suppressing amygdala kindling. Rats were stimulated once daily until fully kindled (stage 5) seizures had developed. Vigabatrin (10 microg) was injected 24 h before the first stimulation as well as 6 h before the 5th and 10th stimulation, which approximately doubled the number of stimulations required for kindling development compared with controls. This marked retardation of kindling acquisition was predominantly due to a significant inhibition of the progression from stage 1 to stage 2 and stage 3 to stage 4 seizures, demonstrating that microinjection of vigabatrin into the central PC markedly inhibits the progression and secondary generalization of focal seizures emanating from the amygdala.

摘要

梨状皮层(PC)是哺乳动物嗅觉皮层中最大的区域,与包括杏仁核、海马体和内嗅皮层在内的边缘系统结构有紧密联系。先前在啮齿动物中的各种研究表明,PC在边缘系统点燃(即颞叶癫痫的一种广泛使用的模型)的发展和维持中可能非常重要。在梨状皮层前后部之间的过渡区(此处称为中央PC)的GABA能抑制似乎特别参与了导致点燃性癫痫发作进展的过程。这促使我们研究通过双侧微量注射氨己烯酸提高梨状皮层该亚区域的GABA水平是否能够抑制杏仁核点燃。每天对大鼠进行一次刺激,直到完全出现点燃(5期)癫痫发作。在第一次刺激前24小时以及第5次和第10次刺激前6小时注射氨己烯酸(10微克),与对照组相比,这使点燃发展所需的刺激次数增加了约一倍。点燃获得的这种显著延迟主要是由于从1期到2期以及从3期到4期癫痫发作的进展受到显著抑制,表明向中央PC微量注射氨己烯酸可显著抑制源自杏仁核的局灶性癫痫发作的进展和继发性泛化。

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