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      Tingenone, a pentacyclic triterpene, induces peripheral antinociception due to cannabinoid receptors activation in mice

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          Most cited references39

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          Ethical guidelines for investigations of experimental pain in conscious animals

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            The endocannabinoid system: its general strategy of action, tools for its pharmacological manipulation and potential therapeutic exploitation.

            The endocannabinoid signalling system includes: (1) at least two G-protein-coupled receptors, known as the cannabinoid CB(1) and CB(2) receptors and discovered following studies on the mechanism of action of Delta(9)-tetrahydrocannabinol, the major psychoactive principle of the hemp plant Cannabis sativa; (2) the endogenous agonists at these receptors, known as endocannabinoids, of which anandamide and 2-arachidonoylglycerol are the best known; and (3) proteins and enzymes for the regulation of endocannabinoid levels and action at receptors. The endocannabinoid system is quite widespread in mammalian tissues and cells and appears to play a pro-homeostatic role by being activated following transient or chronic perturbation of homeostasis, and by regulating in a local way the levels and action of other chemical signals. Compounds that selectively manipulate the action and levels of endocannabinoids at their targets have been and are being developed, and represent templates for potential new therapeutic drugs.
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              Anandamide suppresses pain initiation through a peripheral endocannabinoid mechanism.

              Peripheral cannabinoid receptors exert a powerful inhibitory control over pain initiation, but the endocannabinoid signal that normally engages this intrinsic analgesic mechanism is unknown. To address this question, we developed a peripherally restricted inhibitor (URB937) of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of the endocannabinoid anandamide. URB937 suppressed FAAH activity and increased anandamide levels outside the rodent CNS. Despite its inability to access brain and spinal cord, URB937 attenuated behavioral responses indicative of persistent pain in rodent models of peripheral nerve injury and inflammation and prevented noxious stimulus-evoked neuronal activation in spinal cord regions implicated in nociceptive processing. CB₁ cannabinoid receptor blockade prevented these effects. These results suggest that anandamide-mediated signaling at peripheral CB₁ receptors controls the access of pain-related inputs to the CNS. Brain-impenetrant FAAH inhibitors, which strengthen this gating mechanism, might offer a new approach to pain therapy.
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                Author and article information

                Journal
                Inflammopharmacology
                Inflammopharmacol
                Springer Science and Business Media LLC
                0925-4692
                1568-5608
                February 2018
                September 9 2017
                February 2018
                : 26
                : 1
                : 227-233
                Article
                10.1007/s10787-017-0391-7
                86a97d79-c1bb-4ac9-a317-c0248190d40b
                © 2018

                http://www.springer.com/tdm

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