Department of Physiology and Pathophysiology, Logistics University of Chinese People's Armed Police Force, Tianjin 300162, PR China.
Neuroscience. 2013 Aug 6;244:31-41. doi: 10.1016/j.neuroscience.2013.03.061. Epub 2013 Apr 6.
Perinatal undernutrition affects the hippocampus, a brain region crucial for learning and memory. However, far less is known about the changes of dendritic spine density and morphology related to hippocampal synaptic plasticity. As dendritic spines are dynamic structures essential for synaptic plasticity and serve as the primary post-synaptic location of the excitatory neurotransmission that underlies learning and memory, the aim of the present study was to investigate whether the perinatal undernutrition affected hippocampal synaptic plasticity accompanied by the change of dendritic spines in anesthetized rats. An input-output curve was first determined using the measurements of field excitatory postsynaptic potential (fEPSP) slope in response to a series of stimulation intensities. Long-term potentiation (LTP) induced by high-frequency stimulation was recorded in the Schaffer collateral-CA1 pathway. Post-tetanic potentiation derived from the fEPSP slope was also measured immediately after LTP induction. Quantitative data of dendritic spines from hippocampal CA1 pyramidal cells were obtained using Golgi staining. The results showed that 50% perinatal food restriction (FR50) impaired the magnitude of LTP of the fEPSP slope in the Schaffer collateral-CA1 pathway. Additionally, FR50 reduced overall spine densities in both basal dendrites and apical dendrites of hippocampal CA1 pyramidal cells. Moreover, FR50 reduced type densities of thin and mushroom spines in apical dendrites, whereas a reduction in the type of mushroom spines was only observed in the basal dendrites of hippocampal CA1 pyramidal cells. These findings suggested that perinatal undernutrition decreased excitatory synaptic input and further affected the processing of information in a given network by selectively reducing the number of special dendritic spines. Thus, these changes in the density and the types of dendritic spines in CA1 pyramidal neurons may partly explain the impaired hippocampal synaptic plasticity as well as learning and memory disturbances commonly observed during undernourished rats.
围产期营养不良会影响海马体，海马体是学习和记忆的关键大脑区域。然而，人们对与海马突触可塑性相关的树突棘密度和形态变化知之甚少。由于树突棘是突触可塑性所必需的动态结构，并且作为兴奋性神经递质传递的主要后突触位置，该研究旨在探讨围产期营养不良是否会影响海马突触可塑性，同时伴随着麻醉大鼠树突棘的变化。首先通过测量场兴奋性突触后电位（fEPSP）斜率对一系列刺激强度的反应来确定输入-输出曲线。在 Schaffer 侧枝-CA1 通路中记录高频刺激诱导的长时程增强（LTP）。在 LTP 诱导后立即测量来自 fEPSP 斜率的强直后增强。使用 Golgi 染色获得海马 CA1 锥体神经元树突棘的定量数据。结果表明，50%围产期限食（FR50）损害了 Schaffer 侧枝-CA1 通路中 fEPSP 斜率的 LTP 幅度。此外，FR50 降低了海马 CA1 锥体神经元基底和顶树突中总棘密度。此外，FR50 降低了顶树突中细和蘑菇形棘的类型密度，而仅观察到海马 CA1 锥体神经元基底树突中蘑菇形棘的类型减少。这些发现表明，围产期营养不良减少了兴奋性突触输入，并通过选择性减少特殊树突棘的数量进一步影响了特定网络中的信息处理。因此，CA1 锥体神经元中树突棘密度和类型的这些变化可能部分解释了海马突触可塑性受损以及营养不良大鼠中常见的学习和记忆障碍。
