化学
阈下传导
钾
维尔达格利普汀
药理学
内分泌学
医学
2型糖尿病
物理
量子力学
电压
晶体管
有机化学
糖尿病
作者
Ya He,Fei Wang,Hongxia Zhang,Jingang Li,Hui Zhou,Yuetao Wen
标识
DOI:10.1016/j.neulet.2024.137970
摘要
The subthreshold A-type potassium current (Isa), mediated by Kv4, is a hyperpolarizing current that decreases neuronal excitability. The Kv4 accessory proteins, DPP6 and DPP10 (DPPs), modulate the current. Thus, agents that modify the binding of DPPs to these channels affect neuronal excitability. Vildagliptin inhibits DPP4, a protein with structural similarities to DPPs. In this study, we investigated whether vildagliptin, an antidiabetic medication, exhibits anti-epileptic properties. Seizures were induced in rats by injecting pentylenetetrazole (PTZ), and vildagliptin at different doses was administered one hour before the PTZ injection. Vildagliptin treatment delayed the onset of epileptiform activity and reduced seizure duration and frequency. A dose-dependent decrease in DPPs was observed in vildagliptin-treated rats. We induced epileptic activity in cultured hippocampal neurons and found that treatment with vildagliptin suppressed the firing frequency. We found that the Isa current in cultured neurons was mediated by Kv4s and suppressed in epileptic neurons. Furthermore, the Kv4s to DPPs ratio in the channel complex was decreased in epileptic neurons, but was restored to a normal level in vildagliptin-treated neurons. In conclusion, the anti-epileptic effects of vildagliptin were likely mediated by the suppression of seizure-induced DPP6 and DPP10 expression and decreased membrane excitability by restoring Isa current density via the regulation of DPPs and Kv4s binding, indicating that vildagliptin may be a novel treatment option for epileptic patients.
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