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.

早期研究报告说，慢性严重应激会诱导海马中CA3锥体神经元的树突状萎缩和神经丧失。假设情绪障碍患者将具有遗传确定的压力和异常神经可塑性的脆弱性。据认为，上述海马中应力诱导的神经损伤将在抑郁状态下发生，从而导致情绪障碍的海马少体积损失。我们关于这一假设的问题是，Fisher 344大鼠是一种容易发生情绪障碍的慢性压力的动物模型，是否会通过弱慢性压力显示河马锥体金字塔神经元的形态学改变。 Fisher 344只大鼠连续7或14天承受6小时的约束应力，因为据报道Sprague-Dawley大鼠在6小时的约束压力中显示了CA3神经元的树突状萎缩21天，但没有14天。最后一次约束应力后24小时，Fisher 344只大鼠被深度麻醉和灌注。剖析了含有海马或杏仁核的组织块，并处理高尔基浸渍技术。确定了杏仁核基底外侧核中锥体和星状神经元的CA1，CA3锥体神经元的树突长度，分支点数和脊柱密度，CA3锥体神经元以及脊柱神经元的脊柱密度。 7天和14天的折射应力对CA1和CA3锥体神经元中树突形态的参数没有任何影响。然而，14天的折射应力降低了杏仁核基底外核中星状神经元的脊柱密度。