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The extinction of aversive memories has been of considerable interest for as long as the brain has been known to store memories. Conditions like post-traumatic stress disorder (PTSD) can produce vivid traumatic memories and flashbacks; ideally, if a system could be found to help extinguish these memories, patients would improve much more rapidly and some of the burden of powerful aversive memories could be lifted. CBD has already been identified as a possible therapy for anxiety and insomnia, and even to some degree, with flashbacks associated with PTSD.
This paper explores the role of the endocannabinoid system in memory formation and extinction. The CB1 receptor was deleted from test mice genomes and their phenotype was found to be deficient in the extinction of short and long term memories but normal in acquisition of memories, implying that CB1 is crucial in the extinction of memories.
Here is the full scientific article if you wish to download it.
Further tests reinforced this hypothesis by comparing wild-type mice and CB1-deficient mice. It is proposed that endocannabinoids “facilitate extinction of aversive memories through their selective inhibitory effects on local inhibitory networks in the amygdala”. Therapies are some time away and a lot more work needs to be done.
The formation and extinction of memories is a complex and little understood process. This paper provides for the first time evidence that the relatively newly discovered endocannabinoid system is crucial to this process. When mice without CB1 mice were bred and tested for their memory extinction capabilities, they were found to be deficient in this area. They did, however, form memories normally, suggesting that CB1 is only involved in the extinction of memories.
Further investigation found raised levels of endocannabinoid expression in the basolateral amygdala complex, an area previously proven to be involved in the extinction of aversive memories. The proposed mechanism for this effect is through depression of GABA mediated inhibitory circuits.
Although this is very preliminary data, the commonality between human endocannabinoid systems, memory formation circuitry, and general biology means that these results can be extrapolated to humans with a degree of certainty. Aversive memory extinction is common to basically every creature with a brain, so we can assume that if it is true for mice, it probably will be true for humans. However, the brains of humans are substantially more complex than those of mice, and our memories are thought to be better, so it is unclear at this time.
The therapeutic applications of cannabinoids are multiple and varied. They are known to be tolerable and safe, even at relatively high concentrations. This existing experimental data can be added to the potential of using cannabinoids to affect the extinction of memories. The mechanisms by which this effect is achieved need to be elucidated first, but there is substantial potential for helping people with conditions like PTSD and other forms of trauma.
This study is a preliminary, pre-clinical trial on a small scale. It shows some exciting results but a great deal more work needs to be carried out before any solid conclusions about the role of endocannabinoids in memory extinction can be made. Cannabinoids are known to affect the formation of memories (but apparently the CB1 receptor is not involved), and the mechanisms by which memories are made are far from being understood, so it will be some considerable time before endocannabinoid therapy for aversive therapies will be available, if they do ever reach that stage.
While only a small, initial study, the results are very promising for another therapeutic pathway available to cannabinoids. Currently, the extinction of memories is a relatively unknown process, this study sheds some light on the process and highlights the use of the endocannabinoid system for therapy, but it is a long way from being conclusive. More research is needed.