Background： The pathophysiology of poststroke depression （PSD） remains elusive because of its proposed multifactorial nature. Accumulating evidence suggests that brain-derived neurotrophic factor （BDNF） plays a k...Background： The pathophysiology of poststroke depression （PSD） remains elusive because of its proposed multifactorial nature. Accumulating evidence suggests that brain-derived neurotrophic factor （BDNF） plays a key role in the pathophysiology of depression and PSD. And the cerebellar dysfunction may be important in the etiology of depression; it is not clear whether it also has a major effect on the risk of PSD. This study aimed to explore the expression of BDNF and high-affinity receptors tyrosine kinase B （TrkB） in the cerebellum of rats with PSD. Methods： The rat models with focal cerebral ischemic were made using a thread embolization method. PSD rat models were established with comprehensive separate breeding and unpredicted chronic mild stress （UCMS） on this basis. A normal control group, depression group, and a stroke group were used to compare with the PSD group. Thirteen rats were used in each group. Immunohistochemistry and reverse transcription-polymerase chain reaction （RT-PCR） for detecting the expression of BDNF and TrkB protein and mRNA in the cerebellum were used at the 29th day following the UCMS. Results： Compared with the normal control group and the stroke group, the number of BDNF immunoreactive （IR） positive neurons was less in the PSD group （P 〈 0.05）. Furthermore, the number ofTrkB 1R positive cells was significantly less in the PSD group than that in the normal control group （P 〈 0.05）. The gene expression of BDNF and TrkB in the cerebellum of PSD rats also decreased compared to the normal control group （P 〈 0.05）. Conclusions： These findings suggested a possible association between expression of BDNF and TrkB in the cerebellum and the pathogeuesis of PSD.展开更多
基金Acknowledgments We would like to thank Dr. Tricia for her invaluable comments in the writing of this manuscript. I This research- was supported by a grant from the Yunnan Natural Science Foundation （No. 2009ZC126M）.
文摘Background： The pathophysiology of poststroke depression （PSD） remains elusive because of its proposed multifactorial nature. Accumulating evidence suggests that brain-derived neurotrophic factor （BDNF） plays a key role in the pathophysiology of depression and PSD. And the cerebellar dysfunction may be important in the etiology of depression; it is not clear whether it also has a major effect on the risk of PSD. This study aimed to explore the expression of BDNF and high-affinity receptors tyrosine kinase B （TrkB） in the cerebellum of rats with PSD. Methods： The rat models with focal cerebral ischemic were made using a thread embolization method. PSD rat models were established with comprehensive separate breeding and unpredicted chronic mild stress （UCMS） on this basis. A normal control group, depression group, and a stroke group were used to compare with the PSD group. Thirteen rats were used in each group. Immunohistochemistry and reverse transcription-polymerase chain reaction （RT-PCR） for detecting the expression of BDNF and TrkB protein and mRNA in the cerebellum were used at the 29th day following the UCMS. Results： Compared with the normal control group and the stroke group, the number of BDNF immunoreactive （IR） positive neurons was less in the PSD group （P 〈 0.05）. Furthermore, the number ofTrkB 1R positive cells was significantly less in the PSD group than that in the normal control group （P 〈 0.05）. The gene expression of BDNF and TrkB in the cerebellum of PSD rats also decreased compared to the normal control group （P 〈 0.05）. Conclusions： These findings suggested a possible association between expression of BDNF and TrkB in the cerebellum and the pathogeuesis of PSD.
