Issue release date: 12.11.2024
2Sichuan University, West China Hospital, Department of Neurosurgery, Chengdu, Sichuan, 610041, China
3The Third Military Medical University, Department of Neurobiology, Shapingba District, Chongqing, 400038, China DOI : 10.5137/1019-5149.JTN.13533-14.1 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.
Keywords : Epilepsy, TrkB, GLT-1, Pentylenetetrazol (PTZ), Astrocyte