The expression of NT-3 and TrkC in prefrontal cortex of the post-stroke depression model rats
10.3760/cma.j.issn.1674-6554.2017.12.002
- VernacularTitle:神经营养因子3与酪氨酸激酶受体C在卒中后抑郁模型大鼠额前皮质的表达
- Author:
Yun LI
1
;
Shu LI
;
Wei WANG
;
Ning YANG
;
Yangchao LI
Author Information
1. 大理大学第一附属医院神经内科
- Keywords:
Post-stroke depression;
Prefrontal cortex;
Neurotrophin-3;
Tyrosine kinase re-ceptors C
- From:
Chinese Journal of Behavioral Medicine and Brain Science
2017;26(12):1064-1069
- CountryChina
- Language:Chinese
-
Abstract:
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.