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 embolization method.PSD 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 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). 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 statistical 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). The expression of TrkC in the prefrontal 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 pathogenesis of PSD. Key words: Post-stroke depression; Prefrontal cortex; Neurotrophin-3; Tyrosine kinase receptors C
Published Version
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