Pertussis toxin and voltage dependence distinguish multiple pathways modulating calcium channels of rat sympathetic neurons

Neuron. 1992 Jan;8(1):97-106. doi: 10.1016/0896-6273(92)90111-p.

Abstract

Agonist-induced suppression of current in voltage-gated Ca2+ channels was studied in rat sympathetic neurons. We have previously distinguished two intracellular signaling pathways used by muscarinic agonists to suppress neuronal Ca2+ current-one fast and membrane delimited, the other slow and acting via a diffusible second messenger. We now show that the fast pathway is sensitive mainly to pertussis toxin and shifts the gating of Ca2+ channels to more positive voltages (voltage dependent). The slow pathway is pertussis toxin insensitive and depresses currents at all test potentials (voltage independent). Muscarinic agonists may also activate a pertussis toxin-insensitive fast pathway. alpha-Adrenergic agonists use the fast pertussis toxin-sensitive and the fast insensitive pathways, but not the slow one.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adrenergic alpha-Agonists / pharmacology
  • Animals
  • Calcium Channels / physiology*
  • Electrophysiology
  • GTP-Binding Proteins / physiology
  • Ion Channel Gating / physiology
  • Male
  • Neurons / physiology*
  • Norepinephrine / pharmacology
  • Oxotremorine / pharmacology
  • Pertussis Toxin*
  • Rats
  • Rats, Inbred Strains
  • Receptors, Muscarinic / physiology
  • Sympathetic Nervous System / physiology*
  • Virulence Factors, Bordetella / pharmacology*

Substances

  • Adrenergic alpha-Agonists
  • Calcium Channels
  • Receptors, Muscarinic
  • Virulence Factors, Bordetella
  • Oxotremorine
  • Pertussis Toxin
  • GTP-Binding Proteins
  • Norepinephrine