Gamma-aminobutyric acid and brain-derived neurotrophic factor content in the brain structures of rats with alcohol dependence and under exercise.

The state of alcohol dependence is usually accompanied by emotional disorders, such as anxiety, depression, and aggressiveness. They arise against the background of disturbances in central neurotransmission and neurotrophic processes. Exercise is effective in restoring some damaged brain functions. The aim of our work was to identify disturbances in the g-aminobutyric acid (GABA) and brain-derived neurotrophic factor (BDNF) regulatory systems and the possibilities of their correction by exercise in rats with alcohol dependence. Alcohol dependence was modeled by ingesting food with alcohol at a dose of 1.25 g/kg body weight for 30 days, followed by alcohol withdrawal for 10 days. In rats under alcohol withdrawal, we found an imbalance of GABAergic activity between the frontal neocortex, hippocampus, and amygdala, a decrease in BDNF concentrations in the frontal neocortex, hippocampus, and serum, accompanied by increased anxiety levels. Wheel running during alcohol withdrawal (30 min daily for 10 days) restored the balance of GABA content in the brain structures and the reduced levels of BDNF (excluding reduced GABA and BDNF content in the frontal neocortex), and also reduced anxiety. Exercise increased hippocampal weight, which was decreased in alcohol-dependent animals. The negative correlation was found between indices of hippocampal weight and GABA concentration in hippocampus in intact and alcohol-dependent animals, which persisted even after exercise. The findings suggest that exercise is effective in restoring GABAergic and BDNF signaling impaired by alcohol intake. Restoration of synchronizing GABAergic regulation and BDNF levels contributes to anxiety reduction in alcohol-dependent rats. [ABSTRACT FROM AUTHOR]