机构地区:[1]大理大学第一附属医院神经内科,大理671000 [2]大理大学临床医学院,大理671000
出 处:《中华行为医学与脑科学杂志》2017年第12期1064-1069,共6页Chinese Journal of Behavioral Medicine and Brain Science
基 金:云南省科技厅科研基金项目(2009ZC126M)
摘 要:目的 探讨神经营养因子3(neurotrophic factor-3,NT-3)及其受体酪氨酸激酶受体C (tyrosine kinase receptors,TrkC)mRNA及蛋白在脑卒中后抑郁(post stroke depression,PSD)模型大鼠额前皮质的表达变化.方法 将实验大鼠进行行为学评分(Open-field法),评分相近的大鼠被分为4组:正常组、抑郁组、卒中组及PSD组,每组13只.抑郁组:采用孤养法结合慢性不可预见的中等应激刺激(chronic unpredictable mild stress,CUMS)建立;卒中组:利用线栓法建立局灶性脑缺血大鼠模型;PSD组:动物建成脑缺血模型后孤养再加以CUMS方法建立PSD模型,并与正常对照组、卒中组及抑郁组作比较.于造模后第29天应用免疫组化及RT-PCR检测各组大鼠额前皮质NT-3及其高亲和力受体TrkC的免疫阳性细胞及mRNA的表达情况.结果 免疫组化实验结果发现,PSD组额前皮质NT-3免疫阳性细胞数[(10.11±2.89)个/视野]较正常对照组明显减少[(19.00±12.41)个/视野] (P〈0.05),其余各组相比差异无统计学意义(P〉0.05);PSD组大鼠额前皮质TrkC免疫阳性细胞数[(19.56±5.66)个/视野]较正常对照组[(25.11±3.95)个/视野]及脑卒中组[(29.67±7.38)个/视野]明显减少(P〈0.05);抑郁组免疫阳性细胞数[(19.00±5.61)个/视野]也较正常对照组[(25.11±3.95)个/视野]及脑卒中组(29.67±7.38个/视野)明显减少(P〈0.05);其余各组相比差异无统计学意义(P〉0.05).RT-PCR检查结果显示各组大鼠额前皮质组织中均有 GAPDH、NT3和 TrkCmRNA的表达, PSD组大鼠额前皮质NT-3的表达明显低于正常对照组(P〈0.05);其余各组比较差异无统计学意义(P〉0.05);各组TrkCmRNA表达差异无统计学意义(P〉0.05).结论 PSD大鼠额前皮质NT-3及其受体TrkC的表达减少可能与PSD发病有关.Objective To explore the expression of NT-3 and high-affinity receptors TrkC at mRNA and protein level in the prefrontal cortex of the post stroke depression(PSD)model rats.Methods Open-field method was used to evaluate the behavior.Focal cerebral ischemic rat models were made with thread em-bolization method.PSD rat models were established with comprehensive separately breeding and chronic un-predicted mild stress(CUMS)on this basis.Normal control group,depression group and stroke group were used to compare with PSD group.13 rats were used in each group.At 29th day after the CUMS RT-PCR was employed to detect gene expression of NT-3 and TrkC.The expression of NT-3 and TrkC in positive cells was detected by immunohistochemistry.Results The immunohistochemistry results showed that the number of NT-3 immunopositive cells in PSD group(10.11± 2.89)was lower than that of the normal group(19.00 ± 12.41)(P〈0.05).Whereas there was no statistical difference in the other groups(P〉0.05).The number of TrkC immunopositive cells in PSD group(19.56±5.66)was less than that of the normal group(25.11±3.95) and stroke group(29.67±7.38).The number of TrkC immunopositive cells in depression group(19.00±5.61)also was lower than that of the normal group(25.11±3.95)and stroke group(29.67±7.38).There was no sta-tistical difference among other groups(P〉0.05).RT-PCR results showed that the GAPDH,NT-3 and TrkC mRNA in all of the groups could be detected in the prefrontal cortex of rats.The expression of NT-3 in the prefrontal cortex in the PSD group decreased significantly compared with that of normal control rats(P〈0.05).There was no statistical difference in the other groups(P〉0.05).The expression of TrkC in the pre-frontal cortex had no statistical difference in all of the groups(P〉0.05).Conclusion The down-regulation of NT-3 and TrkC both at mRNA and protein levels in the prefrontal cortex maybe responsible for the pathogen-esis of PSD.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...