Neuronal platelet-activating factor receptor signal transduction involves a pertussis toxin-sensitive G-protein

Gary D. Clark, Charles F. Zorumski, Robert S. McNeil, Leo T. Happel, Ty Ovella, Shannon McGuire, Gregory J. Bix, John W. Swann

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

In most nonneural systems, platelet-activating factor (PAF) receptor effects are mediated by G-proteins that are often pertussis toxin-sensitive. The activation of pertussis toxin-sensitive G-proteins linked to PAF receptors results in the mobilization of intracellular calcium, at least in part, through the second messenger inositol triphosphate. We have sought to determine if a pertussis toxin-sensitive G-protein is involved in the PAF receptor-mediated phenomena of growth cone collapse and of synaptic enhancement in primary neuronal culture. Using infrared differential interference contrast microscopy and patch-clamp recording techniques, pertussis toxin, but not the inactive B oligomer of the toxin, was found to block both the growth cone collapse and the enhanced synaptic release of excitatory transmitter induced by a nonhydrolyzable PAF receptor agonist, making it likely that G(o), G(q), or G(i) is the G-protein transducer of PAF receptors in primary neurons. We believe that PAF acts directly on neuronal receptors, which are linked to pertussis toxin-sensitive G-proteins, on the tips of developing neurites, and on presynaptic nerve terminals, leading to growth cone collapse and enhanced synaptic release of transmitter.

Original languageEnglish
Pages (from-to)603-611
Number of pages9
JournalNeurochemical Research
Volume25
Issue number5
DOIs
StatePublished - 2000

Keywords

  • Axonal growth cone
  • G-protein
  • Growth cone collapse
  • Metabotropic receptor
  • Miniature excitatory post-synaptic currents (MESCS)
  • PAF
  • Pertussis toxin
  • Platelet-activating factor
  • Presynaptic nerve terminal
  • Synaptic plasticity

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