Study for stress-induced morphological alterations of neural dendrites in Fisher344 rats, an animal model for stress-vulnerability

压力脆弱性动物模型 Fisher344 大鼠应激诱导神经树突形态变化的研究

基本信息

批准号：
17591215
负责人：
WATANABE Yoshifumi
金额：
$ 2.24万
依托单位：
Yamaguchi University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

项目摘要

Early studies have reported that chronic severe stress induced dendritic atrophy and neural loss of CA3 pyramidal neurons in the hippocampus. It is hypothesized that mood disorder patients would have the genetically determined vulnerability to stress and aberrant neural plasticity. It is considered that the stress-induced neural damages in the hippocampus described above would occur during a depressive state leading to loss of hippoccampal volume in mood disorders. Our question regarding to this hypothesis is whether Fisher 344 rats, an animal model with the vulnerability to chronic stress for mood disorders, will show morphological alterations of hippoccampal pyramidal neurons by weak chronic stress. Fisher 344 rats were subjected to 6 hours restraint stress daily for 7 or 14 consecutive days, since Sprague-Dawley rats were reported to show the dendritic atrophy of CA3 neurons by 6 hours restraint stress for 21 days, but not for 14 days. Fisher 344 rats were deeply anesthetized and perfused 24 hours after the last restraint stress. Blocks of tissue containing the hippocampus or amygdala were dissected and processed for Golgi impregnation technique. Dendritic length, branch point numbers, and spine density of CA1, CA3 pyramidal neurons in the hippocampus, and spine density of pyramidal and stellate neurons in the basolateral nucleus of amygdala were determined. 7 day-and 14 day-restraint stress did not show any effects on the parameters of dendritic morphology in both CA1 and CA3 pyramidal neurons. However, 14 days-restraint stress decreased the spine density of the stellate neurons in the basolateral nucleus of the amygdala.

早期研究报道，慢性严重应激会导致海马 CA3 锥体神经元的树突萎缩和神经损失。据推测，情绪障碍患者的基因决定了其对压力的脆弱性和异常的神经可塑性。据认为，上述压力诱发的海马神经损伤会发生在抑郁状态期间，导致情绪障碍中海马体积的损失。关于这一假设，我们的问题是，Fisher 344 大鼠（一种容易因慢性应激而导致情绪障碍的动物模型）是否会因微弱的慢性应激而表现出海马锥体神经元的形态变化。 Fisher 344 大鼠每天受到 6 小时的束缚应激，连续 7 或 14 天，因为据报道 Sprague-Dawley 大鼠在 21 天的 6 小时的束缚应激下显示出 CA3 神经元的树突萎缩，但 14 天没有出现这种情况。 Fisher 344 只大鼠在最后一次束缚应激后 24 小时进行深度麻醉和灌注。解剖并处理含有海马或杏仁核的组织块，用于高尔基体浸渍技术。测定海马CA1、CA3锥体神经元的树突长度、分支点数和棘密度，以及杏仁核基底外侧核锥体和星状神经元的棘密度。 7 天和 14 天的束缚应激对 CA1 和 CA3 锥体神经元的树突形态参数没有显示出任何影响。然而，14 天的束缚应激降低了杏仁核基底外侧核中星状神经元的棘密度。