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Opioid Pharmacology of Acute and Chronic Pain

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Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 130))

Abstract

Although it is well established that exogenously administered opiates attenuate nocifensive responses to nociceptive stimuli of various modalities, it has only recently been demonstrated that endogenous opioids exert tonic activities which can either inhibit nociceptive sensory input under normal conditions, or perhaps increase the sensitivity to sensory input in pathological states. Conditions of chronic pain are known to induce a variety of changes in spinal levels and activities of endogenous peptides including enkephalins and dynorphin, in other regulatory neuropeptides such as cholecystokinin (CCK), and in the receptors for these substances. These changes in neuropeptide levels and activity have strong implications in the etiology of chronic pain states and, critically, are likely to be a major factor in determining the outcome of analgesic therapy. For example, reduced spinal CCK content associated with peripheral inflammation has been suggested to result in an increase in the antinociceptive potency of morphine. Conversely, neuropathic pain states are thought to be associated with increased spinal CCK content and, accordingly, reduced antinociceptive potency and efficacy of morphine. Spinal levels of dynorphin are also thought to be increased in conditions of chronic pain.

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Ossipov, M.H., Malan, T.P., Lai, J., Porreca, F. (1997). Opioid Pharmacology of Acute and Chronic Pain. In: Dickenson, A., Besson, JM. (eds) The Pharmacology of Pain. Handbook of Experimental Pharmacology, vol 130. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60777-6_12

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