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Physiological Reviews, Vol. 81, No. 1, January 2001, pp. 299-343
Copyright ©2001 by the American Physiological Society
Vollum Institute, Oregon Health Sciences University, Portland, Oregon; Department of Pharmacology and The Medical Foundation, University of Sydney, Sydney, New South Wales, Australia; and Centre National de la Recherche Scientifique, Unité de Propre de Recherche 9023, Montpellier, France
Williams, John T.,
MacDonald J. Christie, and
Olivier Manzoni.
Cellular and Synaptic Adaptations Mediating Opioid
Dependence. Physiol. Rev. 81: 299-343, 2001.
Although
opioids are highly effective for the treatment of pain, they are also
known to be intensely addictive. There has been a massive research
investment in the development of opioid analgesics, resulting in a
plethora of compounds with varying affinity and efficacy at all the
known opioid receptor subtypes. Although compounds of extremely high
potency have been produced, the problem of tolerance to and dependence
on these agonists persists. This review centers on the adaptive changes
in cellular and synaptic function induced by chronic morphine
treatment. The initial steps of opioid action are mediated through the
activation of G protein-linked receptors. As is true for all G
protein-linked receptors, opioid receptors activate and regulate
multiple second messenger pathways associated with effector coupling,
receptor trafficking, and nuclear signaling. These events are critical
for understanding the early events leading to nonassociative tolerance
and dependence. Equally important are associative and network changes
that affect neurons that do not have opioid receptors but that are
indirectly altered by opioid-sensitive cells. Finally, opioids and
other drugs of abuse have some common cellular and anatomical pathways.
The characterization of common pathways affected by different drugs,
particularly after repeated treatment, is important in the
understanding of drug abuse.
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