Activation of the body’s cannabinoid receptors through spinal infusion is effective at blocking pain, according to a new study published by the journal Regional Anesthesia and Pain Medicine.
“Cannabinoid receptors (CB1R/CB2R) are known to play important roles in pain transmission”, begins the study’s abstract. “In this study, we investigated the effects of continuous intrathecal infusion of CB1/2R agonists in the L5/6 spinal nerve ligation pain model.” Intrathecal infusion is a form of administration for drugs via an injection into the spinal canal, or into the subarachnoid space so that it reaches the cerebrospinal fluid. A CB1/2R agonist is something that activates the cananbinoid receptors, which is done naturally by cannabis and cannabinoids.
Under isoflurane anesthesia, “rats received nerve ligation and intrathecal catheter connected to an infusion pump”. After surgery, saline and three forms of cannabinoid receptor agonists was given intrathecally for 7 days. The mechanical and thermal sensitivities of rat hindpaw were determined by von Frey hair and radiant heat tests. The expression of CB1/2R and protein levels of CB1/2R, Iba1, glial fibrillary acidic protein, and tumor necrosis factor α were examined by immunofluorescence study and Western blotting.
According to researchers, on postligation day 7, rats that received the cannabinoid receptor agonists “had significantly higher mean withdrawal thresholds (6.8, 8.4, and 10.2 g) and latencies (6.3, 7.3, and 9.1 seconds) than did saline-treated rats (1.7 g, 2.2 seconds)”. In addition; “Cannabinoid receptor agonists enhanced nerve ligation-induced up-regulation of cannabinoid receptor in spinal cord and dorsal root ganglion”. Treatment with two of the three agonists “markedly reduced nerve ligation-induced up-regulation of Iba1, glial fibrillary acidic protein, and tumor necrosis factor α in spinal cord.”
Researchers conclude that; “Continuous intrathecal infusion of CB1/2R agonists elicits antinociception [the action or process of blocking the detection of a painful or injurious stimulus by sensory neurons] in the pain model. The mechanisms might involve their actions on neurons and glial cells. CB2R, but not CB1R, seems to play an important role in the regulation of nerve injury-induced neuroinflammation.”
The full study, epublished ahead of print by the U.S. National Institute of Health, can be found by clicking here.