Abstract
The locus coeruleus (LC) contains the largest clusters of noradrenergic neurons in the brain. Single-cell recordings in rats show that LC neurons can be inhibited by clonidine acting via alpha-2 adrenoceptors; morphine and opiate peptides are also inhibitory but act via separate opiate receptors. During states of opiate withdrawal LC neurons become hyperactive; under these conditions clonidine can normalize activity via alpha-2 adrenoceptors even when opiate receptors are blocked. These single-cell studies provide a possible mechanism for the clinical efficacy of clonidine in relieving the signs and symptoms of opiate withdrawal in human addicts.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Clonidine / pharmacology
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Dendrites / physiology
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Evoked Potentials / drug effects
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Humans
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Locus Coeruleus / physiology*
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Morphine / pharmacology
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Neural Inhibition / drug effects
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Neurons / physiology
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Norepinephrine / physiology*
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Piperoxan / pharmacology
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Receptors, Adrenergic / physiology*
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Receptors, Adrenergic, alpha / drug effects
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Receptors, Adrenergic, alpha / physiology*
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Receptors, Opioid / drug effects
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Receptors, Opioid / physiology*
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Synapses / physiology
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Synaptic Transmission / drug effects
Substances
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Receptors, Adrenergic
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Receptors, Adrenergic, alpha
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Receptors, Opioid
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Morphine
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Piperoxan
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Clonidine
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Norepinephrine