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Apamin 诱导老年 Sprague-Dawley 大鼠海马神经元产生可塑性变化。

Apamin induces plastic changes in hippocampal neurons in senile Sprague-Dawley rats.

机构信息

Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Universidad Autónoma de Puebla, CP 72570, Puebla, Puebla, México.

出版信息

Synapse. 2011 Oct;65(10):1062-72. doi: 10.1002/syn.20938. Epub 2011 May 3.

DOI:10.1002/syn.20938
PMID:21465567
Abstract

Apamin is a neurotoxin extracted from honey bee venom and is a selective blocker of small-conductance Ca²⁺-activated K⁺ channels (SK). Several behavioral and electrophysiological studies indicate that SK-blockade by apamin may enhance neuron excitability, synaptic plasticity, and long-term potentiation in the CA1 hippocampal region, and, for that reason, apamin has been proposed as a therapeutic agent in Alzheimer's disease treatment. However, the dendritic morphological mechanisms implied in such enhancement are unknown. In the present work, Golgi-Cox stain protocol and Sholl analysis were used to study the effect of apamin on the dendritic morphology of pyramidal neurons from hippocampus and the prefrontal cortex as well as on the medium spiny neurons from the nucleus accumbens and granule cells from the dentate gyrus (DG) of the hippocampus. We found that only granule cells from the DG and pyramidal neurons from dorsal and ventral hippocampus were altered in senile rats injected with apamin. Our research suggests that apamin may increase the dendritic morphology in the hippocampus, which could be related to the neuronal excitability and synaptic plasticity enhancement induced by apamin.

摘要

蜂毒素是从蜜蜂毒液中提取的一种神经毒素,是小电导钙激活钾通道(SK)的选择性阻断剂。几项行为和电生理研究表明,蜂毒素对 SK 的阻断可能增强 CA1 海马区神经元的兴奋性、突触可塑性和长时程增强,因此,蜂毒素被提议作为阿尔茨海默病治疗的一种治疗剂。然而,这种增强所暗示的树突形态机制尚不清楚。在本工作中,我们使用高尔基-考克斯染色法和邵尔分析研究了蜂毒素对来自海马和前额叶皮质的锥体神经元以及来自伏隔核的中间神经元和来自海马齿状回(DG)的颗粒细胞的树突形态的影响。我们发现,只有注射蜂毒素的老年大鼠的 DG 颗粒细胞和背侧和腹侧海马的锥体神经元发生了改变。我们的研究表明,蜂毒素可能增加海马中的树突形态,这可能与蜂毒素诱导的神经元兴奋性和突触可塑性增强有关。

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