Cannabinoids suppress inflammatory and neuropathic pain by targeting α3 glycine receptors
Chronic pain, particularly neuropathic pain, is a major clinical problem that is difficult to treat (Zhuo, 2007). Despite an intensive search for new analgesics in the last several decades, the need for novel therapeutic strategies remains unmet because virtually every blockbuster drug for the treatment of chronic pain produces aversive side effects (Mogil, 2009; Harrison, 2011). Marijuana has been used to treat chronic pain for thousands of years (Burns and Ineck, 2006; Murray et al., 2007). However, the widespread use of medical marijuana is still controversial because the plant produces both therapeutic and psychoactive effects. Marijuana consists of ∼400 chemical compounds, and ∼60 of them are structurally related cannabinoids. Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) among cannabinoids are major psychoactive and nonpsychoactive components of marijuana, respectively (Howlett et al., 2002; Costa, 2007). There is strong evidence suggesting that nonpsychoactive cannabinoids can also alleviate chronic inflammatory and neuropathic pain in animals (Costa et al., 2007; Izzo et al., 2009). Several recent clinical studies have demonstrated that combination of THC and CBD can be an effective therapeutic option for patients with neuropathic pain and other types of chronic pain (Nurmikko et al., 2007; Turcotte et al., 2010; Lynch and Campbell, 2011). However, there is a need to improve the efficacy and tolerability of these agents in treating chronic pain. One primary obstacle to development of these agents is the uncertainty about the molecular targets for cannabinoid-induced analgesic effects. For instance, the role of spinal CB1 receptors (CB1Rs) in the pain process is debatable. Some studies suggest that activation of CB1Rs in the spinal dorsal horn can facilitate pain (Pernía-Andrade et al., 2009; Zhang et al., 2010; Zeilhofer et al., 2012). Notably, THC-induced analgesia in the tail flick reflex, a test for nociceptive pain threshold, remains intact in mice devoid of CB1 receptors (CB1−/−; Zimmer et al., 1999; Howlett et al., 2002).
Read the entire study here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3371734/
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