Rufinamide Mitigates Seizures and Behavioural Deficits via BDNF/TrkB Modulation and Oxidative Stress Reduction in Pentylenetetrazole‐Kindled Mice

Sep 17, 2025Clinical and experimental pharmacology & physiology

Rufinamide may reduce seizures and behavior problems by affecting brain growth signals and lowering oxidative stress in mice with induced epilepsy

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Abstract

Rufinamide at a dose of 90 mg/kg maximally suppressed full-bloom seizures in PTZ-kindled mice.

Rufinamide decreased cortical epileptic spike discharge in a dose-dependent manner.
Significant anxiolytic effects were observed, preventing PTZ-induced cognitive decline.
The treatment reduced lipid peroxidation and increased levels of antioxidants like glutathione and superoxide dismutase in the brain.
Rufinamide suppressed the PTZ-induced increase in BDNF/TrkB signalling and lowered pro-inflammatory cytokines.
Decreased oxidative stress and neuroinflammatory markers may contribute to the observed effects on seizure activity and neuropsychiatric outcomes.

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BACKGROUND: Rufinamide (RUF) is a 3rd generation antiseizure medication (ASM) with a triazole ring that blocks voltage-gated sodium channels (VGSCs) and is most commonly used to treat Lennox-Gastaut syndrome. Thus, the present study examined the effect of RUF on EEG activity, behavioural testing, oxidative stress, and mRNA expression in PTZ-kindled mice.

METHODS: Male BALB/c mice were administered rufinamide (30, 60, and 90 mg/kg) for 21 days along with 11 injections of PTZ (40 mg/kg) given every other day. EEG recordings were monitored and a series of behavioural tests after RUF treatment were done to assess the post-kindling associated anxiety and memory impairment. We also assessed the oxidative alterations, variation in real-time BDNF/TrkB mRNA expression as well as neuroinflammatory markers in isolated mice brains.

RESULTS: Analysis of results showed that RUF at the dose of 90 mg/kg maximally suppressed the progression of full-bloom seizures and decreased cortical epileptic spike discharge. Moreover, RUF showed significant anxiolytic action and prevented PTZ-induced cognitive decline in a dose-dependent manner. Because of its anti-inflammatory and antioxidant properties, RUF decreased lipid peroxidation, AChE activity, raised glutathione and superoxide dismutase levels in the mice brain. RUF suppressed the PTZ-induced upregulation of BDNF/TrkB signalling and significantly reduced pro-inflammatory cytokines.

CONCLUSION: It is possible that the effects of RUF that have been seen are the consequence of decreased oxidative stress, BDNF/TrkB downregulation, and reduced expression of neuroinflammatory markers, which in turn reduce ictogenesis and improve the neuropsychiatric consequences associated with epilepsy.

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Rufinamide Mitigates Seizures and Behavioural Deficits via BDNF/TrkB Modulation and Oxidative Stress Reduction in Pentylenetetrazole‐Kindled Mice

Abstract

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