Interactive effects of stress and aging on structural plasticity in the prefrontal cortex.
Interactive effects of stress and aging on structural plasticity in the prefrontal cortex.
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DOI：
10.1523/jneurosci.0759-10.2010
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发表时间：
2010-05-12
期刊：
影响因子：
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通讯作者：
Morrison JH
中科院分区：
文献类型：
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作者：
Bloss EB;Janssen WG;McEwen BS;Morrison JH
前额叶皮层中的神经元网络介导最高水平的认知处理和决策，并且执行这些功能的能力是最容易受到衰老影响的认知特征之一。尽管有很多研究，但与年龄相关的前额叶功能受损的神经生物学基础仍然难以捉摸。许多研究人员假设，暴露于压力可能会加速认知老化，但很少有研究直接验证这一假设，甚至更少的研究了这种影响的神经基础。众所周知，在幼年动物中，应激导致前额叶锥体神经元的形态学重塑，这是可逆的。本研究旨在确定年龄是否影响应激诱导的大鼠前额叶神经元形态可塑性的可逆性。我们假设，新皮质结构弹性在正常老化中受到损害。为了直接检验这一假设，我们利用了一个良好的特点慢性约束压力的范例，与一个额外的组允许恢复的压力范例，在3，12和20个月大的雄性大鼠。在年轻的动物中，应力诱导的顶端树突长度和分支数量的减少，这与恢复逆转;相反，中年和老年大鼠未能表现出可逆的形态重塑时，受到相同的应力和恢复范例。这里提出的数据提供的证据表明，老化是伴随着选择性损伤的长期新皮层形态可塑性。
Neuronal networks in the prefrontal cortex mediate the highest levels of cognitive processing and decision making, and the capacity to perform these functions is among the cognitive features most vulnerable to aging. Despite much research, the neurobiological basis of age-related compromised prefrontal function remains elusive. Many investigators have hypothesized that exposure to stress may accelerate cognitive aging, though few studies have directly tested this hypothesis and even fewer have investigated a neuronal basis for such effects. It is known that in young animals, stress causes morphological remodeling of prefrontal pyramidal neurons that is reversible. The present studies sought to determine whether age influences the reversibility of stress-induced morphological plasticity in rat prefrontal neurons. We hypothesized that neocortical structural resilience is compromised in normal aging. To directly test this hypothesis we utilized a well-characterized chronic restraint stress paradigm, with an additional group allowed to recover from the stress paradigm, in 3, 12 and 20-month old male rats. In young animals, stress induced reductions of apical dendritic length and branch number, which were reversed with recovery; in contrast, middle-aged and aged rats failed to show reversible morphological remodeling when subjected to the same stress and recovery paradigm. The data presented here provide evidence that aging is accompanied by selective impairments in long-term neocortical morphological plasticity.