Impairment of synaptic plasticity in hippocampus is exacerbated by methylprednisolone in a rat model of traumatic brain injury

Impairment of synaptic plasticity in hippocampus is exacerbated by methylprednisolone in a rat model of traumatic brain injury
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在创伤性脑损伤大鼠模型中,甲泼尼龙加剧海马突触可塑性损伤

DOI:
10.1016/j.brainres.2011.01.065
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发表时间:
2011-03-25
期刊:
影响因子:
2.9
通讯作者:
Zhang, Jianning
Zhang, Jianning
中科院分区:
医学3区
文献类型:
--
作者:
Zhang, Baoliang;Chen, Xin;Zhang, Jianning

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患有创伤性脑损伤(TBI)的患者表现出认知能力受损,甲基强的松龙(MP)使其恶化。由于长时程增强(LTP)是一个领先的细胞模型的基础学习,我们假设,MP干扰海马的电生理特性,减少创伤后在齿状回(DG)和角ammonis 3(CA 3)地区的inteeneurons的数量,导致学习障碍。为了验证这一假设,我们研究了学习能力的改变,并与海马突触可塑性的变化接受侧向液压冲击损伤(FPI),并与MP治疗的大鼠。我们发现,MP能改善FPI大鼠DG和CA 1区的空间学习障碍和兴奋性变化。功能和电生理缺陷与小清蛋白免疫反应(PV-IR)和胆囊收缩素免疫反应(CCK-IR)GABA能细胞数量减少有关。提示MP治疗可减少创伤后海马DG中间神经元的数量,从而加重TBI所致的学习能力障碍。(C)2011 Elsevier B. V.保留所有权利。
Patients with traumatic brain injury (TBI) exhibit impaired cognitive capability that is exacerbated with methylprednisolone (MP). Since long-term potentiation (LTP) is a leading cellular model underlying learning, we hypothesize that MP disturbs the electrophysiological character in the hippocampus by decreasing the number of inteneurons post-traumatically in the dentate gyrus (DG) and cornu ammonis3 (CA3) regions, resulting in learning deficits. To test this hypothesis, we investigated the alterations of learning abilities and correlated the alternation with hippocampal synaptic plasticity in rats receiving lateral fluid percussion injury (FPI) and being treated with MP. We found that MP aggravates the spatial learning deficiency and changes in the excitability of the DG and cornu ammonis1 (CA1) areas in rats subjected to FPI. The functional and electrophysiological deficits are associated with a decrease in the number of parvalbumin-immunoreactive (PV-IR) and cholecystokinin-immunoreactive (CCK-IR) GABAergic cells. The data suggest that MP therapy may decrease the number of DG interneurons in post-traumatic hippocampus, resulting in the aggravated deficits of learning ability induced by TBI. (C) 2011 Elsevier B.V. All rights reserved.