脑卒中后抑郁大鼠额前皮质脑源性神经营养因子和酪氨酸激酶受体B蛋白的表达变化

The expression of brain-derived neurotrophic factor and tropomyosin receptor kinase B protein in the pre- frontal cortex of the post-stroke depression in the rat model

目的 探讨脑卒中后抑郁（PSD）大鼠额前皮质脑源性神经营养因子（BDNF）和其高亲和力受体酪氨酸激酶B（TrkB）蛋白的表达变化.方法 利用线栓法制备局灶性脑缺血大鼠模型、加以慢性不可预见的中等应激刺激和孤养方法造成PSD动物模型,并与正常对照组、脑卒中组及抑郁组作比较.每组6只动物,应用免疫组化检测各组大鼠造模后第29天大脑额前皮质BDNF和TrkB阳性细胞数的表达变化.结果 PSD组额前皮质BDNF阳性细胞数最少[（21.00±12.41）个/视野]；但各组相比差异无统计学意义（P＞0.05）.PSD组大鼠额前皮质TrkB阳性细胞数最少[（20.78±7.20）个/视野],抑郁组次之[（21.00±5.61）个/视野],脑卒中组最多[（31.67 ±7.38）个/视野]；单因素方差分析结果显示PSD组和抑郁组与脑卒中组比较,均差异有统计学意义（P＜0.05）.结论 PSD大鼠额前皮质TrkB蛋白的表达减少可能与PSD发病机制直接相关.

Objective To explore the expression of brain-derived neurotrophic factor（BDNF） and highaffinity receptors tropomyosin receptor kinase B（TrkB） protien in the prefrontal cortex of the post stroke depression in the rats.Methods Focal cerebral ischemic rat models were made with thread embolization method.Post stroke depression rat models were established with comprehensive separately breeding and chronic unpredicted mild stress （CUMS） on this basis.Normal control group,depression group and stroke group were used to compared with PSD group.6 rats were used in each group.Immunohistochemistry for detecting the expression of BDNF and TrkB in the prefrontal was used at 29th day since the CUMS.Results The number of BNDF immunopositive cells in PSD group was the least （（21.00 ± 12.41） per microscope field of vision） than other groups.Whereas there was no statistical difference among groups（P〉 0.05）.The number of TrkB immunopositive cells in the prefrontal cortex in PSD group was the least （20.78 ± 7.20） among three groups,and depreesion group was secondary （21.00 ±5.61）.Stroke group has the most number of immunopositive cells（31.67 ± 7.38） in the prefrontal cortex among four groups.One way ANOVA statistical analysis showed the number of TrkB immunopositive cells decreased significantly in the PSD group and depression group compared with stroke group （P〈0.05）.Conclusion The downregulation of TrkB immunopositive cells in the prefrontal cortex may be responsible for the pathogenesis of PSD.