Analysis of the Expressions of TrkB and GLT-1 in Brain Tissues on a Rat Pentylenetetrazol Kindling Model of Chronic Epilepsy.

AIM Tyrosine kinase receptor-B (TrkB), a high-affinity receptor for brain-derived neurotrophic factor (BDNF), functions via specific binding with the BDNF. Although studies have shown that BDNF promotes the expression of glutamate transporter-1 (GLT-1) in the glial cells during neurodegeneration, evidence is lacking regarding whether BDNF/TrkB pathway is associated with the abnormal function of GLT-1.The aim of this study is to analyze the expressions of TrkB and GLT-1 in the brain of pentylenetetrazol (PTZ) kindling model of chronic epilepsy in rats, and to provide evidence for the correlation between the BDNF/TrkB pathway and GLT-1 and clues for the prevention and treatment targets of epilepsy. MATERIAL AND METHODS In total, 40 Sprague-Dawley rats were randomly classified as model (n= 30) and control (n= 10) groups respectively. Western blotting was used for analyzing the expression of TrkB and GLT-1, and double immunofluorescence staining was used for detecting the cells positive for both glial fibrillary acidic protein (GFAP) and TrkB in the hippocampus and temporal cortex 7 days after establishing the kindling model. RESULTS Compared with the control group, protein level expression of TrkB and GLT-1, and mean optical density (OD) value of the cells positive for both GFAP and TrkB in the hippocampus and temporal cortex were significantly increased after the onset of epilepsy (P < 0.05). CONCLUSION The BDNF/TrkB pathway may participate in the epileptogenesis through modulating the biological effect of GLT-1 in the glial cells of PTZ kindling rats, though the specific mechanisms require further investigations.