Effects of chronic stress on contextual fear conditioning and the hippocampal expression of the neural cell adhesion molecule, its polysialylation, and L1
Effects of chronic stress on contextual fear conditioning and the hippocampal expression of the neural cell adhesion molecule, its polysialylation, and L1
复制标题
DOI：
10.1016/s0306-4522(00)00484-x
复制
发表时间：
2001-01-01
期刊：
影响因子：
3.3
通讯作者：
Venero, C
中科院分区：
文献类型：
--
作者：
Sandi, C;Merino, JJ;Venero, C
慢性应激已被证明在海马区诱导时间依赖性的神经变性，范围从可逆性损伤到永久性神经元丢失。这种损伤被认为是在海马体依赖的学习任务中损害认知功能。在这项研究中，我们使用了21天的束缚应激程序，以前报道过诱导CA3锥体细胞顶端树突的可逆性萎缩，以评估在涉及高应激水平的实验条件下(以1 mA的冲击强度作为无条件刺激)，它是否会影响随后的背景恐惧条件反射任务的表现。此外，我们对神经损伤可逆性阶段可能涉及的细胞和分子机制的研究也很感兴趣。免疫球蛋白超家族的细胞黏附分子，如神经细胞黏附分子和LI，是细胞表面的大分子，通过其识别和黏附特性调节细胞与细胞之间的相互作用，已被报道在认知功能中发挥关键作用。这项研究的第二个目的是评估慢性应激是否会调节神经细胞黏附分子、其多唾液酸化和海马区L1的表达。结果表明，慢性压力促进了随后的情景恐惧条件反射。他们还显示，慢性应激大鼠海马神经细胞黏附分子减少，但多唾液酸化表达增加，并有增加L1表达的趋势。综上所述，这些结果支持这样的观点，即21天的慢性应激养生有利于个体发展增强的情景恐惧条件性反应。他们还表明，细胞黏附分子可能在慢性应激暴露导致的海马体结构重塑中发挥作用。(C)2001年IBRO。爱思唯尔科学有限公司出版。版权所有。
Chronic stress has been shown to induce time-dependent neurodegeneration in the hippocampus, ranging from a reversible damage to a permanent neuronal loss. This damage has been proposed to impair cognitive function in hippocampus-dependent learning tasks. In this study, we have used a 21-day restraint stress procedure in rats, previously reported to induce reversible atrophy of apical dendrites of CA3 pyramidal cells, to assess whether it may influence subsequent performance in the contextual fear conditioning task under experimental conditions involving high stress levels (1 mA shock intensity as the unconditioned stimulus). In addition, we were interested in the study of the possible cellular and molecular mechanisms involved in the reversible phase of neural damage. Cell adhesion molecules of the immunoglobulin superfamily, such as the neural cell adhesion molecule and LI, are cell-surface macromolecules that, through their recognition and adhesion properties, regulate cell-cell interactions and have been reported to play a key role in cognitive functioning. A second aim of this study was to evaluate whether chronic stress would modulate the expression of the neural cell adhesion molecule, its polysialylation, and L1 in the hippocampus. The results showed that chronic stress facilitated subsequent contextual fear conditioning. They also showed that chronically stressed rats displayed reduced hippocampal neural cell adhesion molecule, but increased polysialylated expression as well as a trend towards exhibiting increased L1 expression.In summary, these results support the view that a 21-day chronic stress regimen predisposes individuals to develop enhanced contextual fear conditioning responses. They also indicate that cell adhesion molecules might play a role in the structural remodelling that occurs in the hippocampus as a consequence of chronic stress exposure. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.