Department of Neurosurgery, Tianjin Neurological Institute, Tianjin Medical University General Hospital, 154 Anshan Road, Tianjin 300052, PR China.
Brain Res. 2011 Mar 25;1382:165-72. doi: 10.1016/j.brainres.2011.01.065. Epub 2011 Jan 26.
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 interneurons 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.
颅脑损伤（TBI）患者表现出认知能力受损，而甲泼尼龙（MP）会使其恶化。由于长时程增强（LTP）是学习的主要细胞模型，我们假设 MP 通过减少创伤后齿状回（DG）和角状回 3 区（CA3）的中间神经元数量，干扰海马的电生理特性，导致学习缺陷。为了验证这一假设，我们研究了接受侧脑室液压冲击伤（FPI）并接受 MP 治疗的大鼠学习能力的变化，并将其与海马突触可塑性相关联。我们发现，MP 加重了 FPI 大鼠的空间学习缺陷和 DG 及 CA1 区兴奋性的改变。功能和电生理缺陷与颗粒蛋白免疫反应性（PV-IR）和胆囊收缩素免疫反应性（CCK-IR）GABA 能细胞数量减少有关。数据表明，MP 治疗可能会减少创伤后海马 DG 中间神经元的数量，导致 TBI 引起的学习能力受损加剧。
