Peripheral mechanisms of opioid analgesia.

Department of Anaesthesiology and Intensive Care Medicine, Charite Campus Benjamin Franklin, Freie Universität Berlin, Hindenburgdamm 30, 12200 Berlin, Germany. <>
Current Opinion in Pharmacology (Impact Factor: 5.44). 02/2009; 9(1):3-8. DOI: 10.1016/j.coph.2008.12.009
Source: PubMed

ABSTRACT Potent and clinically significant analgesic effects can be brought about by opioids acting outside the central nervous system. Injury and inflammation of peripheral tissues leads to increased synthesis, axonal transport, membrane-directed trafficking and G-protein coupling of opioid receptors in dorsal root ganglion neurons. These events are dependent on neuronal electrical activity, cytokines and nerve growth factor and lead to an enhanced analgesic efficacy of peripherally active opioids. Leukocytes infiltrating inflamed tissue upregulate signal-sequence-encoding mRNA for beta-endorphin and its processing enzymes. Depending on the cell type and stimulus, the opioid release is contingent on extracellular Ca2+ or on release of Ca2+ from endoplasmic reticulum. Analgesia results from inhibition of sensory neuron excitability and of proinflammatory neuropeptide release.

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