ACTION OF KETAMINE ON GAMMA AMINOBUTYRIC ACID RECEPTORS IN THE EXPERIMENTAL MODEL OF DEPRESSION (Atena Editora)

Abstract

According to the World Health Organization (WHO), more than 350 million individuals are affected by depression, being one of the main causes of disability worldwide. Recent studies suggest a deregulation of gamma-aminobutyric acid (GABA) levels, the main inhibitory neurotransmitter amino acid of the central nervous system (CNS), in the pathophysiology of depression. Furthermore, it has been postulated that nitric oxide (NO) released during glutamate uptake is related to depression. Thus, the inhibition of the nitrergic pathway would be related to the activation of GABAergic receptors (GABA A subtype), which could be one of the mechanisms responsible for the antidepressant action of compounds that modulate the activity of these receptors. In this context, studies have shown that ketamine (NMDA receptor antagonist) has antidepressant and anxiolytic effects in behavioral tests. Thus, the present study evaluated the participation of GABA A and GABA B receptors in the antidepressant effect of ketamine on NO levels in the cerebral cortex of mice in the tail suspension test (TSC). Therefore, the research design has a quantitative experimental character to investigate the involvement of the GABAergic system in rats treated with a dose of ketamine (0.5 mg/kg) whose results were compared to those of control animals. The presented results demonstrated that the administration of ketamine produced an antidepressant effect on TSC. These results indicate that the effect of ketamine on TSC may involve an activation of GABA A receptors and a possible inhibition of GABA B receptors. ketamine + L-arginine. Thus, we conclude that the antidepressant effect of ketamine involves a modulation of the GABAergic system and NO levels in the cerebral cortex.