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消退程序会根据大鼠训练的强度诱导海马CA1区树突棘的修剪。

Extinction procedure induces pruning of dendritic spines in CA1 hippocampal field depending on strength of training in rats.

作者信息

Garín-Aguilar María E, Díaz-Cintra Sofía, Quirarte Gina L, Aguilar-Vázquez Azucena, Medina Andrea C, Prado-Alcalá Roberto A

机构信息

Departamento de Neurobiología Conductual y Cognitiva, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro Qro., México.

出版信息

Front Behav Neurosci. 2012 Mar 16;6:12. doi: 10.3389/fnbeh.2012.00012. eCollection 2012.

DOI:10.3389/fnbeh.2012.00012
PMID:22438840
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3305886/
Abstract

Numerous reports indicate that learning and memory of conditioned responses are accompanied by genesis of dendritic spines in the hippocampus, although there is a conspicuous lack of information regarding spine modifications after behavioral extinction. There is ample evidence that treatments that typically produce amnesia become innocuous when animals are submitted to a procedure of enhanced training. We now report that extinction of inhibitory avoidance (IA), trained with relatively low foot-shock intensities, induces pruning of dendritic spines along the length of the apical dendrites of hippocampal CA1 neurons. When animals are trained with a relatively high foot-shock there is a high resistance to extinction, and pruning in the proximal and medial segments of the apical dendrite are seen, while spine count in the distal dendrite remains normal. These results indicate that pruning is involved in behavioral extinction, while maintenance of spines is a probable mechanism that mediates the protecting effect against amnesic treatments produced by enhanced training.

摘要

大量报告表明,条件反应的学习和记忆伴随着海马体中树突棘的生成,尽管关于行为消退后棘突修饰的信息明显不足。有充分证据表明,当动物接受强化训练程序时,通常会导致失忆的处理变得无害。我们现在报告,用相对较低的足部电击强度训练的抑制性回避(IA)消退,会诱导海马CA1神经元顶端树突全长的树突棘修剪。当动物用相对较高的足部电击进行训练时,对消退具有高度抗性,并且在顶端树突的近端和中间段可见修剪,而远端树突中的棘突数量保持正常。这些结果表明,修剪参与行为消退,而棘突的维持可能是介导强化训练对失忆处理产生保护作用的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d4/3305886/4f15f5fdd84c/fnbeh-06-00012-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d4/3305886/650c5c0148b8/fnbeh-06-00012-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d4/3305886/0bd5188e60e9/fnbeh-06-00012-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d4/3305886/c653fa310bfb/fnbeh-06-00012-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d4/3305886/4f15f5fdd84c/fnbeh-06-00012-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d4/3305886/650c5c0148b8/fnbeh-06-00012-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d4/3305886/0bd5188e60e9/fnbeh-06-00012-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d4/3305886/c653fa310bfb/fnbeh-06-00012-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d4/3305886/4f15f5fdd84c/fnbeh-06-00012-g0004.jpg

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