Delahunty T M, Jiang J Y, Gong Q Z, Black R T, Lyeth B G
Division of Neurosurgery, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298-0693, USA.
J Neurotrauma. 1995 Dec;12(6):1045-57. doi: 10.1089/neu.1995.12.1045.
We have identified alterations in the responses of muscarinic and metabotropic receptors in rat hippocampus that persist for at least 15 days after central fluid percussion injury. This study compares the effect of lateral fluid percussion and central fluid percussion on these responses. Moderate injury was obtained by displacement and deformation of the brain within the closed cranial cavity using a fluid percussion device positioned either centrally or laterally. Carbachol and (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (trans-ACPD)-stimulated polyphosphoinositide (PPI) hydrolysis was assayed in hippocampus from injured and sham-injured controls at 15 days following injury. At 15 days after central fluid percussion traumatic brain injury (TBI), the response to carbachol was enhanced by 30% and the response to trans-ACPD was enhanced by 75% compared to sham-injured animals. At 15 days after lateral fluid percussion TBI the response to trans-ACPD was enhanced by 40% both ipsilateral and contralateral to the side of injury. In contrast, the response to carbachol was enhanced by 29% contralateral to the side of injury but was diminished by 12% ipsilateral to the side of injury. Cresyl violet staining shows no hippocampal cell death after central fluid percussion injury or on the side contralateral to lateral fluid percussion injury but on the ipsilateral side cell death was identified in hippocampal area CA3. Thus, abnormal hippocampal cell signaling through the phosphoinositide pathway occurs in the absence of cell death and may contribute to cognitive impairment.
我们已经确定，大鼠海马体中M型胆碱能受体和代谢型受体的反应变化在中枢性液体冲击伤后至少持续15天。本研究比较了侧方液体冲击和中枢性液体冲击对这些反应的影响。使用位于中央或侧方的液体冲击装置，通过封闭颅腔内脑的移位和变形造成中度损伤。在损伤后15天，对损伤组和假损伤对照组的海马体中卡巴胆碱和（±）-1-氨基环戊烷-反式-1,3-二羧酸（反式-ACPD）刺激的多磷酸肌醇（PPI）水解进行检测。在中枢性液体冲击性脑损伤（TBI）后15天，与假损伤动物相比，对卡巴胆碱的反应增强了30%，对反式-ACPD的反应增强了75%。在侧方液体冲击性TBI后15天，损伤侧同侧和对侧对反式-ACPD的反应均增强了40%。相比之下，损伤侧对侧对卡巴胆碱的反应增强了29%，但损伤侧同侧对卡巴胆碱的反应减弱了12%。甲酚紫染色显示，中枢性液体冲击伤后或侧方液体冲击伤对侧海马体无细胞死亡，但在侧方液体冲击伤同侧海马体CA3区发现了细胞死亡。因此，在没有细胞死亡的情况下发生了通过磷酸肌醇途径的异常海马体细胞信号传导，这可能导致认知障碍。
