The expression of brain-derived neurotrophic factor and tropomyosin receptor kinase B protein in the prefrontal cortex of the post-stroke depression in the rat model
10.3760/cma.j.issn.1674-6554.2013.06.009
- VernacularTitle: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
- Author:
Yun LI
;
Xu GUO
;
Yonggang LI
- Publication Type:Journal Article
- Keywords:
Post stroke depression;
Prefrontal cortex;
Brain derived neurotrophic factor;
Tropomyosin receptor kinase B,Protein
- From:
Chinese Journal of Behavioral Medicine and Brain Science
2013;(6):507-509
- CountryChina
- Language:Chinese
-
Abstract:
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.
