Activation of kappa opioid receptors reduces seizure activity in a dose-dependent way

Abstract

Background Neuropsychiatric disorders are one of the main challenges of human medicine with epilepsy as one of the most frequent. Temporal lobe epilepsy represents the most common type of epilepsies and is often accompanied by marked neuronal degeneration. One main factor that causes neural loss is the excitotoxicity of glutamate, which is copiously released during seizures and hypoxia accompanying seizures. It was also shown that the deletion of prodynorphin in mice and low expression in humans is associated with increased epilepsy vulnerability. Dynorphin targets opioid receptors and in particular the opioid receptor (KOP). The KOP receptors in the hippocampal formation are located in very strategically points for the control of glutamate release and, most importantly, they are not altered under epileptic conditions. Still, the functional background of these neuroprotective effects is not fully understood. The aim of this study was to investigate the influence of KOP agonists on EEG patterns of epileptic mice.