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 conditions 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.
Read report here
Goodbody has no association with the organisation that conducted this research and is not in a position to validate the research methods, results or conclusions of the published article. It is provided for awareness of research available that may be of interest only. Any reader should read a range of articles and research to have a balanced and informed view.
