Abstract
We investigated the effects of intracerebroventricular (i.c.v.) pertussis toxin upon the sensitivity of supraoptic oxytocin neurones to intravenous morphine (1-5000 micrograms/kg) in urethane-anaesthetized rats. The maximal inhibitory capacity of morphine was diminished by prior administration of pertussis toxin. Some cells were tested with both morphine and with the kappa-opioid agonist U50,488 (1-5000 micrograms/kg): U50,488-induced inhibition of firing rate was apparently unimpaired by pertussis toxin pre-treatment. The opioid inhibition of firing rate seen in the absence of and after pertussis toxin pre-treatment was naloxone-reversible. Thus a pertussis toxin-sensitive G protein may mediate the inhibitory action of morphine upon supraoptic putative oxytocin neurones or inputs to them.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
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Action Potentials / drug effects
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Analgesics / pharmacology
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Animals
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Female
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GTP-Binding Proteins / metabolism*
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Injections, Intravenous
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Microinjections
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Morphine / administration & dosage
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Morphine / pharmacology*
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Neurons / drug effects
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Neurons / physiology*
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Oxytocin / physiology*
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Pertussis Toxin*
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Pyrrolidines / pharmacology
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Rats
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Supraoptic Nucleus / drug effects
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Supraoptic Nucleus / physiology*
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Virulence Factors, Bordetella / administration & dosage
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Virulence Factors, Bordetella / pharmacology*
Substances
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Analgesics
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Pyrrolidines
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Virulence Factors, Bordetella
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Oxytocin
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3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
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Morphine
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Pertussis Toxin
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GTP-Binding Proteins