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. 2010 Apr 29;3(5):1335–1347. doi: 10.3390/ph3051335

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© 2010 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

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Proposed model for the interaction of NSAIDs, opioids and cannabinoids in the descending pain control system to induce analgesia. Minus symbols indicate inhibition. Inhibition of the cyclooxygenases (COX) by NSAIDs reduces the synthesis of prostaglandins (PG) and thromboxanes (TX) and thus increases the availability of arachidonic acid (AA). Opioids also increase the availability of AA by activating the phospholipase A₂ via the µ-opioid receptor. Via the 12-lipoxygenases (12-LOX) AA is transformed into hepoxilins, which indirectly inhibit GABA release. By inhibiting COX and FAAH the NSAIDs spare AEA and 2-AG, which bind to the CB1 receptor (The role of the CB2 receptor in this model has not been established.) and thus inhibit GABA release. Removal of inhibition by GABA enhances the activity of output neurons that inhibit pain.