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最大电休克增加了[3H]Ro 5 - 4864与小鼠大脑皮层结合的密度。

Maximal electroshock increases the density of [3H]Ro 5-4864 binding to mouse cerebral cortex.

作者信息

Basile A S, Weissman B A, Skolnick P

机构信息

Laboratory of Neuroscience, NIDDK, Bethesda, MD 20892.

出版信息

Brain Res Bull. 1987 Jul;19(1):1-7. doi: 10.1016/0361-9230(87)90158-4.

DOI:10.1016/0361-9230(87)90158-4
PMID:2820550
Abstract

The effects of chemically and electrically-induced convulsions on the binding of [3H]Ro 5-4864 to peripheral benzodiazepine receptors (PBR) was studied in both peripheral tissues and the central nervous system (CNS). Acute, maximal electroshock (MES) increased the density of PBR in mouse cerebral cortex as evidenced by a 30% increase in the Bmax of this archetypic ligand. These values returned to control levels by 60 minutes after MES treatment. In contrast, thirty and sixty minutes after convulsions induced by Ro 5-4864, strychnine, or pentylenetetrazol, neither the Bmax nor Kd of [3H]Ro 5-4864 binding to mouse cerebral cortical membranes was altered. The increase in [3H]Ro 5-4864 binding to cortex observed 30 minutes after MES was blocked by anticonvulsant doses of phenobarbital, phenytoin and clonazepam. No changes in the characteristics of [3H]Ro 5-4864 binding was observed in cerebellar or hippocampal membranes 30 minutes following acute MES. Further, after long-term MES administration (1 treatment/day, 5 days), no change in PBR density could be detected 30 minutes after the last MES. Finally, while no change in PBR density was noted in the kidneys 30 minutes after the MES, a significant increase in PBR density was seen in the cardiac ventricles. These results demonstrate a selective modulation of PBR density by MES, suggesting that the PBR could be involved in either the generation of seizures or in postictal compensatory processes.

摘要

研究了化学和电诱导惊厥对[3H]Ro 5-4864与外周苯二氮䓬受体(PBR)结合的影响,研究对象包括外周组织和中枢神经系统(CNS)。急性最大电休克(MES)可增加小鼠大脑皮质中PBR的密度,这种原型配体的Bmax增加30%即证明了这一点。MES处理后60分钟,这些值恢复到对照水平。相比之下,在由Ro 5-4864、士的宁或戊四氮诱导惊厥后30分钟和60分钟,[3H]Ro 5-4864与小鼠大脑皮质膜结合的Bmax和Kd均未改变。MES后30分钟观察到的[3H]Ro 5-4864与皮质结合的增加被抗惊厥剂量的苯巴比妥、苯妥英和氯硝西泮阻断。急性MES后30分钟,小脑或海马膜中[3H]Ro 5-4864结合特性未观察到变化。此外,长期给予MES(每天1次,共5天)后,最后一次MES后30分钟未检测到PBR密度变化。最后,虽然MES后30分钟肾脏中PBR密度未观察到变化,但心室中PBR密度显著增加。这些结果表明MES对PBR密度具有选择性调节作用,提示PBR可能参与癫痫发作的产生或发作后的代偿过程。

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Brain Res Bull. 1987 Jul;19(1):1-7. doi: 10.1016/0361-9230(87)90158-4.
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