Effects of tDCS on glutamatergic pathways in epilepsy: neuroprotective and therapeutic potential

Area of Science:

• Neuroscience
• Neurology
• Biochemistry

Background:

• Epilepsy is a chronic neurological disorder marked by recurrent seizures due to abnormal brain electrical activity.
• Oxidative stress and imbalances in neurotransmitters like glutamate and GABA are implicated in epilepsy pathogenesis.
• Kindling models are widely used to study the mechanisms and potential treatments for epilepsy.

Purpose of the Study:

• To investigate the therapeutic effects of transcranial direct current stimulation (tDCS) on epilepsy.
• To assess tDCS impact on oxidative stress markers (total oxidant capacity and total antioxidant capacity) and key neurotransmitters (calcium ions, glutamate, GABA) and receptors (AMPAR1, NMDAR1) in an epilepsy model.
• To evaluate the influence of tDCS on motor and cognitive functions in epilepsy.

Main Methods:

• Utilized a kindling-induced epilepsy model.
• Administered tDCS stimulation therapy.
• Conducted behavioral tests to assess motor and cognitive functions.
• Measured oxidative stress markers (TOC, TAC) and levels of Ca²⁺, glutamate, GABA, AMPAR1, and NMDAR1 in hippocampal tissue.

Main Results:

• PTZ-induced seizures increased TOC, Ca²⁺, glutamate, GABA, AMPAR1, and NMDAR1 levels, while decreasing TAC.
• tDCS treatment significantly reduced Ca²⁺, TOC, glutamate, GABA, AMPAR1, and NMDAR1 levels in epilepsy cohorts.
• tDCS administration led to a notable increase in TAC levels.
• tDCS demonstrated neuroprotective effects on motor and cognitive functions.

Conclusions:

• tDCS exhibits significant neuroprotective effects in epilepsy models.
• tDCS therapy helps to normalize levels of oxidative stress markers and key neurotransmitters/receptors.
• The findings suggest tDCS as a potential therapeutic strategy for managing epilepsy by targeting oxidative stress and neurotransmitter imbalances.