Effects of beforehand serotonin depletion on experimental acute spinal cord injury

雄性Wistar大鼠，体重约300 g。实验组动物腹腔注射5-HT合成抑制剂d，1，-甲酯盐酸盐对氯苯丙氨酸（p-CPA）400 mg/kg，每日1次，连续3天。对照组动物仅接受溶媒给药。在最后一次注射后的第二天，通过在T7处用Sugita动脉瘤夹进行硬膜外压迫3秒来损伤脊髓。通过大鼠后肢运动分级和大鼠能够维持自身的平面倾斜度来评价大鼠的功能恢复。功能恢复：实验组和对照组大鼠在7月后即刻后肢完全瘫痪。一周后，又有了一些动静。平面倾斜度由伤前的90度下降到伤后的50度.脊髓损伤的组织学：两组大鼠的坏死性血肿仅局限于损伤部位的中央灰质。HE染色光镜观察显示实验组与对照组脊髓病变大小无差异.胶质细胞酸性蛋白（GFAP）免疫反应阳性星形胶质细胞：实验组损伤部位及其尾侧节段星形胶质细胞GFAP免疫反应阳性率较对照组明显。提示脊髓5-羟色胺的预先耗竭对脊髓损伤后继发性损害几乎没有影响，但有可能在神经修复过程中发挥有利的作用。

Male wistar rats weighting arround 300g were used. Animals in the experimental group were treated with d, 1, -methyl-ester-hydrochloride-p-chlorophenylalanine(p-CPA), a 5-HT synthesis inhibitor drug(400mg/kg) intraperitoneally daily for 3 consecutive days. Animals in the control group were treated with only the vehicle. On the next day after the last injection the spinal cords were injured by extradural compression at T7 for 3 seconds with Sugita aneurysm clip. Functional recovery of the rats was evaluated using motor grades of the hindlimbs and inclination of the plane at which a rat could maintain itself.1. Functional recovery : All rats in the experimental and control groups were completely paralysed in the hindlimbs immediately after the injuly. In a week some flicker of movement returned. The inclination of the plane decreased from 90ﾟ before injury to 50ﾟ after injury.2. Histology of injured spinal cord : The necrotic hemotomas had been exclusively localized in the central gray matter at the injury site in the rats of the both groups. Light microscopic study with HE staining did not show any difference in the size of the cord lesion between the experimental and control group.3. Glial fibrillary acid protein (GFAP) immunoreactive astrocytes : The GFAP immunoreactivity of astrocytes in the injury site and also at the segments caudal to it was more remarked in the experimental group than in the control group. Those results might suggest that beforehand depletion of serotonin in the spinal cord has almost no effect on the secondary damage of the cord following injury but has the possibility of playing a favorable role in neural reparative process.