The aim of this research was to assess the effects of cannabidiol on different targets of the hypothalamus-pituitary-adrenal (HPA) axis under baseline stress conditions. Administered (5mg/kg, 15mg/kg, and 30mg/kg) 90 minutes before single restraint stress exposure, measurements were taken of alterations in the relative gene expressions of corticotropin-releasing factor in the paraventricular nucleus, pro-opiomelanocortin in the arcuate nucleus of the hypothalamus, glucocorticoid receptor in the hippocampus, and serotonin 5-HTR1A receptor in the hippocampus and amygdala.
There were alterations in 5-HTR1A in the amygdala and hippocampus. Cannabidiol successfully blocked the effects induced by acute stress on corticotropin-releasing factor, pro-opiomelanocortin and glucocorticoid receptor gene expression. Additionally, restraint stress induced the opposite effects in 5-HTR1A gene expression in the hippocampus and amygdala. These results combined suggest the ability of cannabidiol to regulate acute stress HPA axis activation might be explained by its action on 5-HTR1A receptors, agonists for which show efficacy in relieving anxiety, depression, and aggression, specifically in the circumstance of stressful situations.
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