In recent times, cannabinoids have emerged as a possible treatment option for stress and anxiety-related disorders such as post traumatic stress disorder (PTSD). A research was aimed to examine whether cannabinoid receptor activation may inhibit the effects of traumatic stress on the development of behavioral and neuroendocrine measures in a rat model of PTSD, the single-prolonged stress (SPS) model.
During the research, rats were injected with the CB1/CB2 receptor agonist WIN55,212-2 (WIN) systemically or into the basolateral amygdala (BLA) at varying time points following SPS exposure and were tested a week later for inhibitory avoidance (IA) conditioning and extinction, acoustic startle response (ASR), hypothalamic-pituitary-adrenal (HPA) axis function, and anxiety levels.
It was revealed that SPS exposure improved conditioned avoidance and impaired extinction while increasing ASR, negative feedback on the HPA axis, and anxiety. WIN (0.5 mg/kg) administered intraperitoneally 2 or 24 h (but not 48 h) after SPS inhibited the trauma-induced alterations in IA conditioning and extinction, ASR potentiation, and HPA axis inhibition. SPS-induced alterations in IA and ASR were prevented by WIN microinjected into the BLA (5 μg/side). The effects were blocked by intra-BLA co-administration of the CB1 receptor antagonist AM251 (0.3 ng/side) and suggested the involvement of CB1 receptors.
It was suggested by the findings that there could be an optimal time-window for intervention treatment with cannabinoids after a highly-stressful event exposure and some preventive effects induced by WIN are possible of being mediated by the activation of CB1 receptors in the BLA. It was also revealed by the research findings that cannabinoids may serve as a pharmacological treatment of stress and trauma-related disorders.
Department of Psychology, University of Haifa, Haifa, Israel