Abstract
Opioids and opiates decrease the duration of action potentials and the amount of neurotransmitter released from sensory neurons. The mu-type opioid receptor, the binding site for morphine, is thought to act exclusively on K+ channels. Here, we show that activation of the mu receptor inhibits Ca2+ channels in rat sensory neurons; the effect is blocked by a mu antagonist and is not mimicked by kappa or delta receptor agonists. Both low-threshold (T-type) and high-threshold Ca2+ currents are partially suppressed. omega-Conotoxin-sensitive and omega-conotoxin-insensitive, high-threshold Ca2+ currents are inhibited. The kinetic effect on high-threshold current is like that caused by diminished rest potential: the transient component is selectively lost, whereas the sustained component is spared.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
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Amino Acid Sequence
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Animals
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Calcium Channels / drug effects
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Calcium Channels / physiology*
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Cells, Cultured
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Electric Conductivity
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Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
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Enkephalin, D-Penicillamine (2,5)-
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Enkephalins / pharmacology
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Molecular Sequence Data
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Mollusk Venoms / pharmacology
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Naltrexone / analogs & derivatives
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Naltrexone / pharmacology
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Narcotic Antagonists
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Pyrrolidines / pharmacology
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Rats
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Receptors, Opioid / drug effects
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Receptors, Opioid / physiology*
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Receptors, Opioid, delta
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Receptors, Opioid, kappa
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Receptors, Opioid, mu
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omega-Conotoxin GVIA
Substances
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Calcium Channels
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Enkephalins
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Mollusk Venoms
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Narcotic Antagonists
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Pyrrolidines
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Receptors, Opioid
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Receptors, Opioid, delta
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Receptors, Opioid, kappa
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Receptors, Opioid, mu
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Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
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Naltrexone
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3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
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beta-funaltrexamine
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Enkephalin, D-Penicillamine (2,5)-
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omega-Conotoxin GVIA