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Journal of Neuroscience, Vol 11, 3830-3839, Copyright © 1991 by Society for Neuroscience
Opiate withdrawal-induced hyperactivity of locus coeruleus neurons is substantially mediated by augmented excitatory amino acid input
H Akaoka and G Aston-Jones
Department of Mental Health Sciences, Hahnemann University, Philadelphia, Pennsylvania 19102.
Single-cell activity was recorded in the locus coeruleus (LC) of
morphine-dependent, halothane-anesthetized rats. Systemic administration of
the opiate antagonist naloxone (0.1 mg/kg, i.v.) robustly increased the
activity of LC neurons. Local microinjection of naloxone or of its
hydrophilic derivative, naloxone methiodide, into LC (10 mM, 20-40 nl) did
not activate LC neurons in dependent rats. Intracerebroventricular or
intracoerulear injection of kynurenate, a broad-spectrum antagonist of
excitatory amino acids (EAAs), substantially but incompletely attenuated
the activation of LC cells induced by intravenous naloxone-precipitated
withdrawal (more than 50% blockade). Intracoerulear microinjections of the
non-NMDA-receptor antagonist 6-cyano-7-dinitroquinoxaline-2,3-dione (CNQX)
or the selective NMDA-receptor antagonist AP5 significantly reduced the
withdrawal-induced excitation. AP5 was the least effective among all
antagonists tested. Similar microinjections of kynurenate or CNQX almost
completely suppressed the excitation of LC neurons induced by electrical
stimulation of a rear footpad. LC responses to footpad stimulation
(mediated by endogenous EAAs) or iontophoretically applied glutamate were
not modified by the chronic morphine treatment. These results indicate that
a substantial part of LC hyperactivity during opiate withdrawal is mediated
by an augmented EAA input to LC.
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