Plastic reorganization of hippocampal and neocortical circuitry in experimental traumatic brain injury in the immature rat
Plastic reorganization of hippocampal and neocortical circuitry in experimental traumatic brain injury in the immature rat
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DOI：
10.1089/neu.2005.22.989
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发表时间：
2005-09-01
影响因子：
4.2
通讯作者：
Adelson, PD
中科院分区：
文献类型：
--
作者：
Card, JP;Santone, DJ;Adelson, PD
在未成熟的前脑电路的重组所造成的控制皮质的影响进行了检查与病毒transneuronal示踪。在出生后第17天（PND）受伤的动物和来自同一窝的假手术对照组在PND 45接受了将伪狂犬病病毒（PRV）重组株脑内注射到内嗅皮层中。注射病毒后50小时，灌注动物，用PRV特异性抗血清免疫化学定位感染的神经元。先前的研究已经证明，在该分析中使用的PRV重组体仅以逆行方向移动通过突触连接的神经元。CCI诱导的皮质坏死损失的影响和变量的损害，基本的胼胝体和喙（背侧）海马，是不存在于假对照组的网站。假手术对照组的病毒转运分析显示，病毒通过海马和新皮质回路的逆行转运模式与已建立的连接和地形图模式一致。受伤的动物在海马和新皮层中表现出地形组织连接的保留。然而，在受伤的半球标记的幅度显着增加，相对于对照组动物，并与损伤的程度。感染神经元在对侧未受伤半球的分布也符合已知的连接。然而，胼胝体在损伤中的参与差异导致了病例中感染神经元数量的更大变化。这些数据提供了新的见解创伤诱导重组的发展中的大脑，并添加到实验工具，可用于评估的基础上功能恢复的动物模型的发育性创伤性脑损伤。
The reorganization of circuitry in the immature forebrain resulting from controlled cortical impact was examined with viral transneuronal tracing. Animals injured on postnatal day (PND) 17 and sham controls from the same litters received an intracerebral injection of a recombinant strain of pseudorabies virus (PRV) into the entorhinal cortex on PND 45. Fifty hours following injection of virus the animals were perfused and infected neurons were localized immunohistochemically with antisera specific for PRV. Prior studies have demonstrated that the PRV recombinant used in this analysis moves exclusively in the retrograde direction through synaptically linked neurons. CCI induced a necrotic loss of cortex at the site of impact and variable damage to the underlying corpus callosum and rostral (dorsal) hippocampus that was not present in sham controls. Analysis of viral transport in sham controls revealed retrograde transport of virus through hippocampal and neocortical circuitry in a pattern consistent with established patterns of connectivity and topography. Injured animals exhibited preservation of topographically organized connections in both the hippocampus and neocortex. However, the magnitude of labeling in the injured hemisphere was significantly increased relative to control animals and correlated with the magnitude of the injury. The distribution of infected neurons in the contralateral uninjured hemisphere also conformed to known connections. However differences in the involvement of the corpus callosum in the injury resulted in greater variability in the number of infected neurons among cases. These data provide novel insights into trauma induced reorganization of the developing brain and add to the experimental tools that can be used to assess the basis for functional recovery in animal models of developmental traumatic brain injury.