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Vol. 297, Issue 1, 11-18, April 2001
Department of Pharmacology and Toxicology, Robert C. Byrd Health
Sciences Center, West Virginia University School of Medicine,
Morgantown, West Virginia
The cellular basis of tolerance to, and dependence upon, many types of
drugs, including opioids, has long defied identification. Tolerance to
opioids cannot be explained solely on the basis of modification of
opioid receptors or altered metabolism or disposition of the opioid.
The development of tolerance following chronic exposure to opioids
presents at least three different types of change in cellular
responsiveness, each of which has been suggested to represent some type
of adaptive modification in cellular responsiveness. These different
forms of tolerance are distinguishable on the basis of their time
course and whether or not the tolerance is specific for opioid receptor
agonists (homologous) or extends to agonists of other systems
(heterologous). The adaptive modulation of responsiveness via
regulation of cellular proteins has been proposed to be the basis for
both longer-term forms of tolerance. The divergent signaling pathways
activated by G-protein-coupled receptors like the µ-opioid receptor
provide multiple downstream targets for both short- and long-term
regulation of cell function that is associated with the development of
tolerance and/or dependence. Since the magnitude of receptor activation
is an important determinant of the degree to which various signaling
pathways are activated, the expressed characteristics of tolerance
and/or dependence may be functionally related to which of these diverse
pathways are stimulated to the greatest degree. Thus, the possibility
that different signaling events are activated either sequentially or concurrently offers the possibility to explain the interaction between
these different forms of tolerance and/or dependence.
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