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Journal of Neuroscience, Vol 16, 2758-2766, Copyright © 1996 by Society for Neuroscience
Spinal amino acid release and precipitated withdrawal in rats chronically infused with spinal morphine
KH Jhamandas, M Marsala, T Ibuki and TL Yaksh
Department of Anesthesia, University of California at San Diego, Ja Jolla 92093-0818, USA.
Glutamate receptors are implicated in the genesis of opioid tolerance and
dependence. Factors governing release of amino acids in systems chronically
exposed to opiates, however, remain undefined. Using rats, each prepared
with a spinal loop dialysis catheter and with a chronic lumbar intrathecal
infusion catheter connected to a subcutaneous minipump, the release of
amino acids before and during antagonist- precipitated withdrawal in
unanesthetized rats was examined. Spinal infusion of morphine (20
nmol/micro l/hr) for 4 d had little effect on resting release of amino
acids. In morphine-infused, but not saline- infused, rats naloxone (2
mg/kg, i.p.) evoked an immediate increase in the release of L-glutamate
(299 +/- 143%) and taurine (306 +/- 113%) but not other amino acids. The
magnitude and time course of the release of these amino acids significantly
correlated with behavioral indices of withdrawal intensity. Acute
intrathecal pretreatment immediately before naloxone with clonidine (20
microg; alpha2 agonist), MK-801 (3 microg; noncompetitive NMDA antagonist),
or aminophosphonopentanoic acid (AP-5; 3 microg; competitive NMDA
antagonist) suppressed naloxone- induced increases in spinal L-glutamate
and taurine release and behavioral signs of withdrawal in spinal
morphine-infused rats. Results point to a correlated increase in spinal
L-glutamate release, which contributes to genesis of the opioid withdrawal
syndrome. Agents such as clonidine that suppress opioid withdrawal may owe
their action to an inhibition of excitatory amino acid release. The effects
of MK-801 and AP-5 suggest a glutamate-evoked glutamate release.
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