本文研究了D 半乳糖对大鼠空间学习记忆行为及对在体诱导海马齿状回LTP的影响

并观察了电针的干预作用。正常组每日皮下注射生理盐水 1mL

模型组和电针组每日皮下注射D 半乳糖 ( 80 0mg/kg)共 6周

电针组从第 1 8天开始电针。空间学习记忆行为以Morris水迷宫潜伏期作为判定标准 ;应用记录单脉冲刺激穿通纤维在海马齿状回诱发的群体电位

测量高频刺激(HFS)前后单脉冲刺激诱发的电位幅值变化

将HFS前的记录作为对照值

进行组间比较。结果显示 :①模型组水迷宫潜伏期成绩明显低于正常组

电针组潜伏期成绩与模型组比显著提高 (P <0 .0 5) ;②HFS前记录显示 :三组间PS潜伏期和PS平均幅值无显著性差异

HFS后

1 0只正常组大鼠有 8只产生了LTP。其电位平均幅值增加为基线值的 1 3 5± 3 .9% ;1 0只模型组大鼠有 2只产生了LTP

其平均值为基线值的 1 2 1 .4± 1 .4% ;电针组 9只大鼠有 5只产生了LTP

其平均幅值为基线值的 1 3 1 .8± 5.3 %。提示 :D 半乳糖可损害大鼠的空间学习记忆能力、降低大鼠在体海马齿状回LTP的诱导率

降低LTP振幅 ;电针可提高模型动物的空间学习记忆能力

阻抑半乳糖对LTP诱导的损害作用Objective:To observe the influence of subcutaneous injection of D galactose on rat spatial learning and memory

induction of LTP in hippocampal dentate gyrus in vivo

and the effect of electroacupuncture (EA). Methods: 33 Wistar rats were randomly divided into normal control group (n=11)

model group (n=11) and EA group (n= 11). In control group

normal saline (1 mL) was given to the rats subcutaneously every day

continuously for 6 weeks. In model group and EA group

subcutaneous injection of D galactose (800 mg/kg/d) was given to the rats daily and continuously for 6 weeks. From the 18th day on EA of ""Baihui"(GV 20) and "Dazhui"(GV 14) (5 mA

10 Hz

15 min) was conducted for rats of EA group. Spatial learning and memory ability was evaluated by latency of Morris water maze. Following anesthesia with 20% urethane 1.0 g/kg(i.p.)

according to Paxinos' Rat Brain Stereotaxic Atlas

a bipolar stimulating electrode was inserted into the site (A: 7.5 mm; R:4.0 mm) 4 mm below the cortex and an induction electrode inserted into the site (A: 3.5 mm

R: 2.0 mm) for recording potentials of hippocampal dentate gyrus. The average value of 20 population spikes (PS) induced by single pulse stimulation of perforate path fiber was used as the baseline value for detecting the changes of potential amplitude before and after high frequency stimulation (HFS). Results: The latency of Morris water maze of model group was longer than that of control group

suggesting impairment of the learning and memory induced by D galactose. Compared with model group

the latency of EA group was significantly shorter

suggesting an inhibitory effect of EA on D galactose injury (P<0.05). Before HFS

no difference was found among the three groups in the latency and the mean amplitude value of PS; while after HFS

in control group

LTP appeared in 8 of 10 rats and the mean amplitude value of PS increased to 135.0±3.9% in comparison with the baseline value. In model group

LTP occurred in 2 of 10 rats and the mean amplitude value of PS increased to 121.4± 1.4%. In EA group

LTP generated in 5 of 9 rats and the mean amplitude value of PS increased to 131.8±5.3%. The incidence of LTP induction of rats in model group was significantly lower than that of control group(P<0.05).The ratio of PS amplitude after HFS 60 min and before HFS in EA group was higher than that of model group(P<0.05). The incidence of LTP was increased in EA group

but had no significant difference. Conclusion: EA can suppress subcutaneous injection of D galactose induced learning and memory impairment

improve its resultant incidence of LTP induction and increase PS amplitude in the rat.