酒精处理影响青春期大鼠海马CA1区BDNF和TrkB的表达

Effects of alcohol treatment on the expression of BDNF and TrkB in CA1 area of hippocampus in adolescent rat

为探讨青春期饮酒致学习记忆力下降的可能机制,本研究观察了青春期大鼠酒精处理后海马CA1区脑源性神经营养因子(BDNF)和酪氨酸激酶受体B(TrkB)的表达变化。实验选用30d龄SD雄性大鼠,以25%的酒精按8g/kg/d灌胃,连续灌7d,动物分别在停酒后0d,3d,7d和14d处死;对照组以等量生理盐水代替酒精按同样方法处理。用免疫组织化学方法(ABC法)检测海马CA1区BDNF和TrkB的表达,Motic3.2图像分析系统测定免疫阳性产物的平均灰度值。结果显示,BDNF的表达在停酒后0d和14d,实验组与相应对照组相比差异无显著性(P>0.05);3d显著升高(P<0.05);7d明显下降(P<0.05)。TrkB的表达在停酒后0d,3d,7d,实验组与相应对照组相比差异无显著性(P>0.05);14d显著下降(P<0.05)。以上结果提示,BDNF表达的相对不足可能是青春期饮酒致学习记忆力持续性下降的原因之一。

To investigate the possible mechanism of adolescent drinking leading to a decline of learning and memory ability, in the present study, we observed the effect of alcohol treatment on the expression of brain-derived neurotrophic factor （BDNF） and tyrosine kinase receptor B （TrkB） in adolescent rat CA1 area of hippoeampus. Male SD rats of 30-day-old were treated with 8 g/kg ethanol （25% V/V ethanol） everyday by intragastrie gavage for 7 consecutive days and were executed respectively at the 0 d, 3 d, 7 d and 14 dafter stopping treatment; control group rats received isovolumetric saline instead of ethanol. BDNF and TrkB expressions in the CA1 area of hippocampus were observed by immunohistochemical technique （ABC method）, and the mean gray values of immunoreactive products were detected by Motic3.2 image analysis system. The results showed that the expression of BDNF had no significant difference between experimental groups and corresponding control groups at the 0 d or 14 d after stopping drinking （ P 〉 0.05 ） , but it was increased significantly 3 d after stopping drinking （ P 〈 0.05 ） and was decreased significantly 7 d after stopping drinking （ P 〈 0. 05 ） compared with their corresponding control groups. There was no significant difference in the expressions of TrkB between experimental groups and the corresponding control groups at the 0 d, 3 d, 7 d after stopping drinking （ P 〉 0.05 ） , but it was decreased significantly 14 d after stopping drinking compared with its corresponding control groups （P 〈0.05）. These results suggest that the relative insufficient expression of BDNF in hippocampal CA1 area may be one of the reasons for the long-term deficits of/earning and memory after alcohol treatment in the adolescent.