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海藻酸损毁小结叶小脑后的行为和受体变化

Behavior and receptor changes after kainate lesioning of nodular cerebellum.

作者信息

Maiti A, Shahid Salles K, Grassi S, Abood L G

出版信息

Pharmacol Biochem Behav. 1986 Sep;25(3):589-94. doi: 10.1016/0091-3057(86)90146-2.

DOI:10.1016/0091-3057(86)90146-2
PMID:3022307
Abstract

A study was undertaken on the effects of kainic acid lesioning on the nodulus of the rat cerebellum on behavior and various brain receptors in conscious, freely moving rats. The basis for the study was the observation that barrel rotation and other motor effects induced by intraventricular administration of vasopressin and nicotine could be elicited by their administration into the nodular area of the cerebellum. Histology revealed a marked destruction of Purkinje, stellate, and Golgi cells in the area surrounding the site of kainate administration, with little effect on the granular cells. Immediately after administering 4-12 ng of kainic acid into the nodular cerebellum, rats exhibited circling movements, barrel rotation, and clonic convulsions accompanied by stereotypic head movements, aggressiveness, and gnawing-biting; effects gradually diminishing over 3 days. Receptor binding studies 4-14 days after kainate lesioning revealed a marked increase in 3H-nicotine and 3H-QNB binding in the surrounding cerebellar region, caudate nucleus, and hypothalamus, with no change in 3H-dihydromorphine binding. The findings are consistent with the hypothesis that nicotinic and muscarinic pathways in the vestibular cerebellum, along with its connection to nigrostriatal dopaminergic systems, are involved in the mediation of barrel rotation, ataxia, and other motor disturbances resulting from administration of vasopressin on nicotine intraventricularly.

摘要

一项关于海藻酸损伤大鼠小脑小结对清醒、自由活动大鼠行为及各种脑受体影响的研究开展了。该研究的依据是观察到脑室内注射血管加压素和尼古丁所诱导的桶状旋转及其他运动效应,可通过将它们注射到小脑小结区域而引发。组织学检查显示,在海藻酸盐注射部位周围区域,浦肯野细胞、星状细胞和高尔基细胞有明显破坏,而颗粒细胞受影响较小。在向小脑小结注射4 - 12纳克海藻酸后,大鼠立即出现转圈运动、桶状旋转和阵挛性惊厥,并伴有刻板的头部运动、攻击性和啃咬行为;这些效应在3天内逐渐减弱。海藻酸损伤后4 - 14天的受体结合研究显示,在小脑周围区域、尾状核和下丘脑,3H - 尼古丁和3H - QNB结合显著增加,而3H - 二氢吗啡结合无变化。这些发现与以下假设一致:前庭小脑的烟碱能和毒蕈碱能通路,连同其与黑质纹状体多巴胺能系统的连接,参与介导脑室内注射血管加压素或尼古丁所导致的桶状旋转、共济失调及其他运动障碍。

相似文献

1
Behavior and receptor changes after kainate lesioning of nodular cerebellum.海藻酸损毁小结叶小脑后的行为和受体变化
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Barrel rotation and prostration by vasopressin and nicotine in the vestibular cerebellum.
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Soman- or kainic acid-induced convulsions decrease muscarinic receptors but not benzodiazepine receptors.梭曼或海藻酸诱发的惊厥会减少毒蕈碱受体,但不会减少苯二氮䓬受体。
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Kainate Receptor-Mediated Depression of Glutamate Release Involves Protein Kinase A in the Cerebellum.红藻氨酸受体介导的小脑谷氨酸释放抑制涉及蛋白激酶 A。
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Postnatal expression of V2 vasopressin receptor splice variants in the rat cerebellum.大鼠小脑V2血管加压素受体剪接变体的产后表达。
Differentiation. 2009 Apr;77(4):377-85. doi: 10.1016/j.diff.2008.11.002. Epub 2009 Jan 20.