癫痫伴抑郁大鼠杏仁核脑源性神经营养因子及其受体酪氨酸激酶受体B的表达观察

Expression of amygdala BDNF and its receptor TrkB in epilepsy-associated depression rats

目的观察癫痫伴抑郁(EAD)大鼠杏仁核脑源性神经营养因子(BDNF)及其受体酪氨酸激酶受体B(TrkB)的表达变化,探讨BDNF及其受体TrkB在EAD发病中的作用。方法将健康成年SD大鼠52只随机分为EAD组、癫痫组、抑郁组和对照组,每组13只。抑郁组采用慢性不可预见的中等应激刺激结合孤养法建立大鼠慢性应激抑郁模型;癫痫组和EAD组采用氯化锂-匹罗卡品建立癫痫模型,于造模后第14天对癫痫模型进行抑郁筛选,癫痫伴发抑郁大鼠为EAD组;癫痫未伴发抑郁大鼠为癫痫组。对照组为健康SD大鼠。于造模成功后第29天(4周后),处死各组大鼠,采用活体灌注取脑法取脑,并分离出脑组织中的杏仁核。应用免疫荧光染色法、Western blotting法检测各组大鼠杏仁核BDNF及TrkB蛋白。结果模型建立成功后第29天,与癫痫组、对照组相比,EAD组大鼠杏仁核BDNF及TrkB表达阳性细胞数均减少(P均<0.05),BDNF和TrkB蛋白表达降低(P均<0.05)。结论与癫痫大鼠比较,EAD大鼠杏仁核BDNF及TrkB表达均降低,二者表达降低可能提示EAD发病。

Objective To observe the expression changes of amygdala brain-derived neurotrophic factor(BDNF)and its receptor tyrosine kinase receptor B(TrkB)in epilepsy-associated depression(EAD)rats,and to investigate the role of BDNF and its receptor TrkB in the pathogenesis of EAD.Methods Fifty-two healthy adult SD rats were randomly divided into the EAD group,epilepsy group,depression group,and control group,with 13 rats in each group.The chronic depression model was established in the depression group by chronic unpredictable moderate stress stimulation combined with orphan method.The epilepsy model was established by lithium chloride-pilocarpine in the epilepsy group and EAD group.The epilepsy model was screened for depression on the 14 th day after modeling,and the epilepsy-associated depression rats were taken as the EAD group,rats with epilepsy without depression were taken as the epilepsy group,and the control group was healthy SD rats.On the 29 th day after the successful modeling(after 4 weeks),the rats in each group were sacrificed,and the brain was obtained by in vivo perfusion and the amygdala in the brain tissue was isolated.The BDNF and TrkB proteins in the amygdala of each group were detected by immunofluorescence staining and Western blotting.Results On the 29 th day after successful model establishment,compared with the epilepsy group and the control group,the number of BDNF and TrkB positive cells in the amygdala of the EAD group decreased(P<0.05),and the expression of BDNF and TrkB protein decreased(both P<0.05).Conclusion Compared with the epileptic rats,the expression of BDNF and TrkB in amygdala of EAD rats decreases,and the decreased expression of both may indicate the pathogenesis of EAD.