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Abstract
Endocannabinoids produced in the spinal cord can enhance pain by dampening the synapses of inhibitory interneurons that usually prevent the perception of innocuous stimuli as painful. This mechanism promotes pain responsiveness to normally innocuous mechanical stimuli in the skin surrounding a site of injury in both animals and humans subjected to sustained stimulation of pain-sensing nerves. The pain-promoting action of endocannabinoids wanes during the development of chronic pain that is induced by inflammation or nerve injury. This finding may partially explain why, in human trials, cannabinoid drugs have been negative for treatment of most types of acute and postsurgical pain but are effective for some chronic pain states.
