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Journal of Xi'an Jiaotong University(Medical Sciences) ; (6): 169-174, 2015.
Artículo en Chino | WPRIM | ID: wpr-461193

RESUMEN

ABSTRACT:Objective To study the BDNF/TrkB signaling pathway in the epilepsy model of hippocampal neurons and the regulatory effect of on it.Methods The primary hippocampal neurons cultured in vitro for 7 days were randomly divided into seven groups:control group,epilepsy group,control+BDNF group,epilepsy+BDNF group,control + miR-185 ? group,epilepsy + miR-185 ? group,and epilepsy + miR-185 ? + BDNF group.We constructed miR-185 ? lentivirus vector and observed the changes of BDNF/TrkB pathway expression after transfaction of miR-185 ? by immunohistochemistry,patch clamp technique and Western blot technique.Results Compared with the control+BDNF group,the phosphorylated TrkB (pTrkB)/TrkB value was significantly lower in epilepsy+BDNF group (P < 0.05 )and control group (P < 0.001 ).Compared with the epilepsy group,the phosphorylated TrkB (pTrkB)/TrkB value was significantly higher in epilepsy+BDNF group (P <0.05).Compared with the epilepsy+miR-185 ? +BDNF group,the phosphorylated TrkB (pTrkB)/TrkB value was significantly lower in epilepsy + BDNF group and epilepsy + miR-185 ? group (P < 0.001 ).BDNF could promote the signaling conduction and miR-185 ? could remove the inhibition of BDNF/TrkB signaling.Conclusion BDNF can activate the BDNF/TrkB signaling pathway and transfection with miR-185 ? can relieve the inhibition of BDNF/TrkB signaling pathway of epileptic state by up-regulating the expression of TrkB.

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