Study: Cannabinoids Prevent the Development of Behavioral and Endocrine Alterations in a Rat Model of Intense Stress

Published: Neuropsychopharmacology, September 14, 2011

Authors: Eti Ganon-Elazar and Irit Akirav, University of Haifa in Israel

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Summary

A 2011 study conducted at the University of Haifa in Israel, and published in the journal Neuropsychopharmacology, suggest that medical marijuana may prevent PTSD. The study exposed 637 male rats to extreme stress-inducing experiences such as restraint, forced swims and anesthetization. After the rats were severely stressed, some were immediately given a synthetic compound that mimics the effects of THC. Those that did not receive the THC injections showed symptoms like humans who develop PTSD: oversensitivity, changes in stress hormone levels, and exaggerated startle response to loud noises. But those that were given THC did not have any of the symptoms of PTSD. However, these results were only if the rats were injected within 24 hours after the traumatic experience, and had no effect when given 48 hours afterwards. These findings suggest that THC may play an important pharmaceutical role in preventing PTSD if taken immediately after a traumatic experience.

 

Abstract

Cannabinoids have recently emerged as a possible treatment of stress- and anxiety-related disorders such as post-traumatic stress disorder (PTSD). Here, we examined whether cannabinoid receptor activation could prevent 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. Rats were injected with the CB1/CB2 receptor agonist WIN55,212-2 (WIN) systemically or into the basolateral amygdala (BLA) at different time points following SPS exposure and were tested 1 week later for inhibitory avoidance (IA) conditioning and extinction, acoustic startle response (ASR), hypothalamic-pituitary-adrenal (HPA) axis function, and anxiety levels. Exposure to SPS enhanced conditioned avoidance and impaired extinction while enhancing 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 prevented the trauma-induced alterations in IA conditioning and extinction, ASR potentiation, and HPA axis inhibition. WIN microinjected into the BLA (5 μg/side) prevented SPS-induced alterations in IA and ASR. These effects were blocked by intra-BLA co-administration of the CB1 receptor antagonist AM251 (0.3 ng/side), suggesting the involvement of CB1 receptors. These findings suggest that (i) there may be an optimal time window for intervention treatment with cannabinoids after exposure to a highly stressful event, (ii) some of the preventive effects induced by WIN are mediated by an activation of CB1 receptors in the BLA, and (iii) cannabinoids could serve as a pharmacological treatment of stress- and trauma-related disorders.