Abnormal Cannabidiol Affects Production of Pro‐Inflammatory Mediators and Astrocyte Wound Closure in Primary Astrocytic‐Microglial Cocultures
In Summary
Damage to the brain such as brain trauma or stroke comprises two consecutive events. The initial one, primary damage, involves loss of neurons. It is then followed by a secondary damage, which is characterized by complex inflammatory cascades that aggravate the initial loss. The inflammatory response is regulated by two types of supporting cells in the brain, microglia and astrocytes. More specifically, while a rapid production and hence increase in the number of astrocytes at the site of damage represents a form of scar forming and wound healing, the simultaneous accumulation of both microglia and astrocytes lead to excessive inflammatory reactions that are associated with secondary damage.
Endocannabinoid is a group of lipids naturally produced by the body, and shares similar structures and functions with cannabinoids derived from plants such as cannabis or synthesized artificially. Compounds in this group exert their effects on the body by binding to and activating cannabinoid receptors on the cells. Recently, scientists discovered a previously unknown cannabinoid receptor that is widely expressed on both microglial cells and astrocytes and regulates their migration and functions. Excitingly, activation of this new receptor was shown to increase blood flow and therefore alleviate damages caused by stroke to the brain in lab rats. Although the mechanism underlying this effect is complicated and needs further research to fully elucidate, scientists suggested this receptor, when activated, reduces accumulation of and attenuate the inflammatory response by microglial cells. It also mediates the reorganization and wound closure reaction of astrocytes.