运动训练对血管性痴呆大鼠学习记忆能力及海马GAP-43表达的影响

The effects of rehabilitation training on learning, memory and expression of GAP-43 in hippocampus CA1 area of rats with vascular dementia

目的研究运动训练对血管性痴呆（VD）大鼠学习记忆功能恢复及组织生长相关蛋白-43（GAP-43）表达的影响。方法选择SD雌性大鼠44只，随机分为运动组20只、制动组20只和假手术组4只，采用双侧颈总动脉反复缺血再灌注加降血压法制作血管性痴呆大鼠模型。运动组大鼠每天进行滚筒、转棒训练，时间为1h；制动组大鼠被限制自由活动；假手术组置于普通笼中自由活动。3组分别于术后第27，28天进行跳台试验测定学习、记忆能力。取脑组织采用免疫组织化学染色方法观察不同时间点海马CA1区GAP．43的表达。结果以跳台试验对学习记忆能力进行的评估示运动组优于制动组（P〈0．01），运动组GAP-43在海马CA1区的表达第1天后逐渐增高，第7天时达高峰，较制动组和假手术组均有明显增加（P〈0．01）。结论运动训练可改善VD大鼠学习记忆能力，其机制可能与运动训练能促进海马CAl区上GAP-43表达有关。

Objective To study the effects of rehabilitation training on learning and memory ability and the expression of growth-associated protein-43 （GAP-43） in rats with vascular dementia. Methods Forty-four female Sprague-Dawley rats were randomly assigned to a rehabilitation group （ n = 20）, an immobilization group （ n = 20） , and a sham-operation group （ n = 4）. The rats in the former 2 groups were operated on to establish the experimental vascular dementia model by repeatedly ischemia/reperfusion injury of brain induced by ligation of bilateral common carotid arteries and lowering of blood pressure induced by intraabdominal injection of sodium nitroprusside. The rats in rehabilitation group were administered with rotating bar and rolling cage exercises for 1 hour once daily, while those in the immobilization group were immobilized and without any exercise; the rats in sham-operation group could move freely in cage. Learning and memory tests were preformed by using step-down avoidance test at the 27th and 28th days after operation. Immunohistochemical staining was used to detect GAP-43 expression in hippocampus CA1 area at different time points after operation. Results The rats in rehabilitation group demonstrated better learning and memory ability than those in immobilization group（P 〈0.01 ） , and more GAP-d3 expression in hippocampns CAI area than those in immobilization group and sham-operation （P 〈 0.01 ）. Conclusion Rehabilitation training can improve the learning and memory ability of rats with experimental vascular dementia, and the mechanism is probably related to the increase of GAP-43 in hippocampus CA1 area.