The role of TRP ion channels and neurotrophic factors in different experimental epilepsy models: investigation with molecular and electrophysiological approaches

Aim: Epilepsy, one of the most common neurological disorders, affects millions of people worldwide. The purpose of this study was to investigate the role of TRP ion channels and some neurotrophic factors in epilepsy by analysing their gene expression in different experimental epilepsy models. Methods: A total of 32 adult Wistar albino and WAG/Rij male rats (n=8) were used in our study, which was approved by the ethics committee. Control, Acute PTZ, Chronic PTZ (Kindling), and Absence Epilepsy groups have been created. A single dose of pentylenetetrazol (PTZ) (50 mg/kg) was given to the animals in the acute model, whereas PTZ (35 mg/kg) was injected intraperitoneally three times a week until the animals' kindling behavior was observed in the chronic PTZ model. The absence epilepsy model causes epileptiform activity on its own. After 60 minutes of electrocorticogram recording from the animals, the cortex and hippocampal tissues were isolated. The real-time polymerase chain reaction method was used to examine the expression levels of the target genes. Using SPSS 20.0 software, the data collected were compared using a one-way analysis of variance post-hoc LSD test. Significant values were those smaller than p<0.05. Results: The expressions of TRPM3, TRPM8, TRPV1, and NGF genes in cortex tissues increased significantly in the absence epilepsy group compared to the control group (p<0.05). In hippocampus, expressions of TRPM2, and TRPM8 genes decreased significantly in the acute PTZ and chronic PTZ groups compared to the control group (p<0.05), TRPM3 and TRPV1 genes were significantly increased in the absence epilepsy group compared to the control group (p<0.05), and NGF gene expression increased significantly in acute PTZ and chronic PTZ groups compared to the control (p<0.05). Conclusion: TRP ion channels and growth factor gene expression levels can be affected differently in different epilepsy models. Increased expression of TRPM3, TRPM8, TRPV1, and NGF genes may play an important role in the pathophysiology of absence epilepsy and cause changes in neural networks. This study brings a new perspective to the literature and contributes to research on epilepsy.