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Vol. 282, Issue 3, 1408-1417, 1997
Department of Pharmacology (C.A.F., G.L.W.),
Graduate
Program in Neuroscience (G.L.W.), University of Minnesota,
Minneapolis, Minnesota
The mechanistic similarity between acutely and chronically induced
morphine tolerance has been previously proposed but remains largely
unexplored. Our experiments examined the modulation of acutely induced
tolerance to spinally administered morphine by agonists that affect the
N-methyl-D-aspartate receptor and nitric oxide synthase
systems. Antinociception was detected via the hot water (52.5°C) tail
flick test in mice. Intrathecal pretreatment with morphine (40 nmol)
produced a 9.6-fold rightward shift in the morphine dose-response
curve. This shift confirmed the induction of acute spinal morphine
tolerance. Intrathecal copretreatment with the receptor antagonists
(competitive and noncompetitive, respectively) dizolcipine (MK801, 3 nmol) or LY235959 (4 pmol) and morphine [40 nmol, intrathecally
(i.t.)] attenuated acute tolerance to morphine measured 8 hr later. A
60-min pretreatment of 7-nitroindazole (6 nmol, i.t.), a selective
neuronal NOS inhibitor, followed by administration of morphine (40 nmol, i.t.) blocked the induction of morphine tolerance. Intrathecal
copretreatment with morphine (40 nmol, i.t.) and agmatine (4 nmol,
i.t.), an imidazoline1 receptor agonist and putative nitric
oxide synthase inhibitor, almost completely abolished acute spinal
morphine tolerance. The results of these experiments agree with
previous reports using models of chronically induced
morphine tolerance. This evidence supports the proposal that the
mechanisms responsible for acute morphine tolerance parallel those
underlying chronic morphine tolerance. This study attests to the
powerful predictive value of acute induction as a model
for morphine tolerance.
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