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The Journal of Neurophysiology Vol. 85 No. 6 June 2001, pp. 2388-2397
Copyright ©2001 by the American Physiological Society
Department of Psychiatry, University of Pennsylvania, Veterans Affairs Medical Center (151), Philadelphia, Pennsylvania 19104
Ivanov, Alexander and
Gary Aston-Jones.
Local Opiate Withdrawal in Locus Coeruleus Neurons In Vitro. J. Neurophysiol. 85: 2388-2397, 2001. Noradrenergic neurons of the brain nucleus locus coeruleus (LC) become
hyperactive during opiate withdrawal. It has been uncertain to what
extent such hyperactivity reflects changes in intrinsic properties of
these cells. The effects of withdrawal from chronic morphine on the
activity of LC neurons were studied using intracellular recordings in
rat brain slices. LC neurons in slices from chronically morphine-treated rats exhibited more than twice the frequency of
spontaneous action potentials after naloxone compared with LC neurons
from control rats. However, after naloxone treatment, the resting
membrane potential (MP) of LC neurons from dependent rats was not
significantly different from that in control rats. Neither resting MP
nor spontaneous discharge rate (SDR) was altered by naloxone in LC
neurons from control rats. Neither kynurenic acid nor a cocktail of
glutamate and GABA antagonists (6-cyano-7-nitroquinoxalene-2,3-dione + 2-amino-5-phosphonopentanoic acid + bicuculline) blocked the hyperactivity of LC neurons precipitated by naloxone in slices from
morphine-dependent rats. The effects of ouabain on MP and SDR were
similar in LC neurons from control and morphine-dependent rats. These
results indicate that an adaptive change in glutamatergic or GABAergic
synaptic mechanisms or altered Na/K pump activity does not underlie the
withdrawal-induced activation of LC neurons in vitro. Specific
inhibitors of protein kinase A [Rp-cAMPS or N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinolinesulfonamide
(H-89)] partially suppressed the withdrawal hyperactivity of
LC neurons, and activators of cAMP (forskolin) or protein kinase A
(Sp-cAMPS) increased the discharge rate of LC neurons from control
rats. These results suggest that upregulation of cAMP-dependent protein kinase A during chronic morphine treatment is involved in the withdrawal-induced hyperactivity of LC neurons.
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