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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诱导海马CA3锥体神经元树突萎缩和神经丧失。据推测，情绪障碍患者可能具有基因决定的对压力的易感性和异常的神经可塑性。我们认为，上述应激性海马神经损伤可能发生在抑郁状态下，导致心境障碍患者海马体积的减少。关于这一假设，我们的问题是，Fisher 344大鼠作为情绪障碍慢性应激易感性的动物模型，是否会在弱慢性应激下表现出海马锥体神经元的形态学改变。Fisher 344大鼠连续7天或14天每天施加6小时约束应激，因为有报道称Sprague-Dawley大鼠在连续21天施加6小时约束应激时CA3神经元出现树突萎缩，但14天没有。Fisher 344大鼠在末次约束应激后24小时深度麻醉灌注。解剖含有海马或杏仁核的组织块，进行高尔基浸渍处理。测定海马CA1、CA3锥体神经元的树突长度、分支点数和脊柱密度，以及杏仁核基底外侧锥体和星状神经元的脊柱密度。7 d和14 d约束应激对CA1和CA3锥体神经元树突形态参数均无影响。然而，14天的约束应激降低了杏仁核基底外侧核星状神经元的脊柱密度。