It is known that perirhinal/insular cortices participate in the transmission of sensory stimuli to the motor cortex, thus coordinating motor activity during seizures. In the present study we analysed seizure-related proteins, such as GABA, glutamate, ERK1/2 and the synaptic proteins in the insular cortex of Krushinsky-Molodkina (KM) rats genetically prone to audiogenic seizures (AGS). We compared seizure-naïve and seizure-experienced KM rats with control Wistar rats in order to distinguish whether seizure-related protein changes are associated with seizure event or representing an inhered pathological abnormality that determines predisposition to AGS. Our data demonstrated an increased level of vesicular glutamate transporter VGLUT2 in naïve and seizure-experienced KM rats, while glutamic acid decarboxylases GAD65 and GAD67 levels were unchanged. Evaluation of the synaptic proteins showed a decrease in SNAP-25 and upregulation of synapsin I phosphorylation in both groups of KM rats in comparison to Wistar rats. However, when phosphorylation level of ERK1/2 in naïve KM rats was significantly increased, several episodes of AGS diminished ERK1/2 activity. Obtained data indicate that changes in ERK1/2 phosphorylation status and glutamate release controlling synaptic proteins in the insular cortex of KM rats could contribute to the AGS susceptibility.
Keywords: ERK1/2; Insular cortex; Krushinsky-Molodkina audiogenic rats; SNAP25; Synapsin I; VGLUT2.