Oral Cannabidiol Prevents Allodynia and Neurological Dysfunctions in a Mouse Model of Mild Traumatic Brain Injury

In conclusion, our data show some of the brain modifications probably responsible for the behavioral phenotype associated with TBI and suggest the CBD as a pharmacological tool to improve neurological dysfunctions caused by the trauma. Introduction The phytocannabinoid cannabidiol (CBD), the major non-psychoactive constituent of Cannabis sativa, exhibits a broad spectrum of potential therapeutic properties, including neuroprotective effects in Central Nervous System (CNS) disorders (Fernández-Ruiz et al., 2013; De Gregorio et al., 2018; Schonhofen et al., 2018). Through a multitarget mechanism, CBD shows potent anti-inflammatory and anti-oxidant properties which have been previously demonstrated in different models of neurodegenerative diseases and in acute episodes of brain damage (i.e., hypoxia-ischemia) (Hayakawa et al., 2007, 2010; Castillo et al., 2010). CBD has very low affinity for cannabinoid receptors type 1 (CB1) and type 2 (CB2), whereas different mechanisms, such as inhibition of anandamide uptake and enzymatic hydrolysis (Lastres-Becker et al., 2005), and decrease of adenosine reuptake (Carrier et al., 2006), are believed to be responsible for its neuroprotective effects. Traumatic brain injury (TBI) is a complex injury with a number of symptoms accompanied by inflammatory process and cell death (Arciniegas, 2011; Liu et al., 2019). It is characterized by an initial neuroinflammation, mediated by a rapid glia cells activation, peripheral immune ce...
Source: Frontiers in Pharmacology - Category: Drugs & Pharmacology Source Type: research

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