| Abstrakt: |
Epilepsy affects many people globally and results from disrupted neuron balance, causing abnormal central nervous system electrical activity. Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) regulation, alongside transient receptor potential (TRP) channel involvement, underscores epilepsy's complexity. This study unveils TRP ion channel and neurotrophic factor expression in epilepsy models for future therapeutic insights. A study with 32 male Wistar albino and WAG/Rij rats was conducted, approved ethically. Groups included Control, PTZ, Kindling, and Absence Epilepsy. PTZ group received a 50 mg/kg dose, Kindling received 35 mg/kg PTZ three times a week. Absence Epilepsy group showed inherent epileptiform activity. After a 60-min electrocorticogram recording, cortex and hippocampal tissues were isolated. Real-time polymerase chain reaction assessed gene expression. Statistical analyses used SPSS.20.0 with a one-way analysis of variance post-hoc LSD test (p < 0.05). In the cortex of Absence Epilepsy, expressions of TRPM3, TRPM8, TRPV1, and NGF genes significantly increased compared to the Control group (p < 0.05). In the hippocampus, both the PTZ and Kindling groups showed significantly decreased expressions of TRPM2 and TRPM8 compared to the Control group (p < 0.05). Furthermore, the hippocampus of the Absence Epilepsy group exhibited significantly elevated expressions of TRPM3 and TRPV1 genes compared to the Control group (p < 0.05), whereas the expression of the NGF gene significantly increased in both PTZ and Kindling groups compared to the Control group (p < 0.05). This study highlights varied effects on TRP ion channels and growth factor gene expression in different epilepsy models. Increased expressions of TRPM3, TRPM8, TRPV1, and NGF genes may contribute significantly to the absence epilepsy pathophysiology, influencing neural network modifications. The findings provide a new perspective to the literature and contribute to ongoing epilepsy research. [ABSTRACT FROM AUTHOR] |
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