Identification of brain areas sensitive to the toxic effects of sparteine

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• 作者：T. Meraz Medina^a ; Jacinto Ba&ntilde ; uelos Pineda^a ; Carmen Cecilia Gó ; mez Rodiles^a ; Salvador Jimé ; nez Vallejo^a ; Ricardo Solí ; s Zamora^b ; Pedro Macedonio Garcí ; a Ló ; pez^b ; ^{pgarcia@cucba.udg.mx}
• 关键词：Quinolizidine alkaloids ; Sparteine toxicity ; Intracranial administration ; Brain
• 刊名：Experimental and Toxicologic Pathology
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：69
• 期：1
• 页码：27-31
• 全文大小：1429 K
• 卷排序：69

文摘

Sparteine is one of the most toxic quinolizidine alkaloids found in leguminous plants. Several studies have demonstrated that sparteine affects the nervous system, blocking the nervous ganglion, producing antimuscarinic effects, depressing the central nervous system and causing neuronal necrosis. However, there are no reports identifying the areas of the brain that are sensitive to the toxic effects of this alkaloid. 32 adult Wistar rats were on study, sixteen were implanted with an intracerebral stainless steel cannula and randomly assigned to a control or experimental group (n = 8). Animals, control and experimental, received daily intraventricular (ICV) injections of a sparteine or a sterile water solution for five consecutive days. Additionally, two groups of animals (8 rats each) received daily intraperotineal injections (IP) of a sparteine or sterile water solution for five consecutive days. 72 h after the last dose, the animals were sacrificed, their brains removed, fixed and embedded in paraffin to obtain 10 μm tissue slices. Brain slices were stained with H&E and evaluated under a light microscope. The main brain structures sensitive to sparteine were the cerebral cortex (frontal, fronto-parietal and striate) olfactory and amygdaloid areas, the ventromedial hypothalamic nucleus, the Purkinje cells in the cerebellum, and the CA1, CA3 and dentate gyrus regions of the hippocampus.Administration of sparteine, via ICV or IP, caused neuronal necrosis in brain structures, mainly related with cholinergic pathways.