According to research presented at the 11th FENS Forum of Neuroscience (7–11 July, Berlin, Germany), teams from Italy and Canada describe their findings that animal models of post-traumatic stress disorder (PTSD) and colitis are regulated by related brain pathways involving naturally occurring cannabis-like compounds, paving the way for new treatment options.
“People with trauma-related stress disorders often turn to cannabis for self-medication and as the law is changing around the use of cannabis in many countries, there has been an upsurge of public interest in its potential therapeutic uses,” explained Patrizia Campolongo (Sapienza University, Rome, Italy).
Looking at rat models of PTSD, Campolongo established that synthetic drugs that augment brain levels of natural cannabinoids can reduce symptoms of trauma while also treating the cognitive dysfunction, and that these effects are long-term.
Campolongo commented: “These drugs work in much more targeted brain areas than street cannabis, and, as long as 3 months after treatment, they stop reinstatement of anxiety symptoms. This equates to several years in man and is of note because PTSD patients often relapse sometime after the end of treatment.”
According to Campolongo, synthetic drugs influencing levels of natural cannabinoids may act both to reduce the symptoms of anxiety (much like classical PTSD treatments) and also break the cycle by which sufferers relive the trauma and thus, continue excessive recall of it.
“These artificial cannabis compounds are very specific, and hence have reduced risk of side effects. We now need to test whether what we have found in animals is the same as in man,” she stated.
In addition to this work, Matthew Hill (Hotchkiss Brain Institute, University of Calgary, Canada) also presents research into the links between inflammatory diseases and stress-associated disorders, which often occur together.
Hill’s work has demonstrated that levels of the brain’s natural cannabis-like molecules are reduced in an animal model of colitis, suggesting that an artificial boost may be necessary and sufficient to alleviate the anxiety associated with this condition.
“We don’t know the mechanism by which these conditions are linked but suspect it may be to do with the body’s endocannabinoid system. We have found, in a rat model of colitis, that levels of a naturally occurring cannabis, anandamide, were reduced in several areas of the brain, probably as a result of increased activity of an enzyme which breaks it down,” Hill commented.
Furthermore, Hill believes that colitis increases levels of a chemical termed CRH, and that this triggers a cycle whereby the enzyme becomes more active, breaking down anandamide and resulting in anxiety. “When we artificially block the activity of CRH, and hence of the enzyme, anandamide levels stay high and the anxiety commonly seen with colitis does not occur,” he remarked.
Both of these works from Campolongo and Hill suggest that well-controlled human studies to assess the medical benefits of cannabis would be valuable in a range of linked conditions.
Sources: Campolongo P. Arousal and stress effects on cannabinoid modulation of memory. Presented at: FENS Forum of Neuroscience, Berlin, Germany, 7–11 July 2018; Hill M. Endocannabinoids: a mechanism of comorbidity between inflammatory disease and anxiety. Presented at: FENS Forum of Neuroscience, Berlin, Germany, 7–11 July 2018; https://forum2018.fens.org/contact-press/press-releases
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