αLatrotoxin of black widow spider venom binds to a specific receptor coupled to phosphoinositide breakdown in PC12 cells

L. M. Vicentini, J. Meldolesi

Research output: Contribution to journalArticle

Abstract

αLatrotoxin of black widow spider is known to bind with high affinity to surface sites of rat pheochromocytoma (PC12) cells, thereby causing depolarization, calcium influx and massive neurotransmitter release. We show here that the toxin causes the accumulation of inositol phosphates, the products of phosphoinositide breakdown. Inositol 1,4,5, trisphosphate was predominantly accumulated shortly after toxin application. Phosphoinositide breakdown appears to be a direct consequence of toxin binding because high K+ and ionophores (which induce depolarization, calcium influx and transmitter release by different mechanisms) were without such effect. Phosphoinositide breakdown is known as an event coupled to the activation of receptors of various hormons and transmitters. We suggest therefore that the αlatrotoxin binding site is a receptor coupled across the membrane to the phosphoinositide hydrolysing system.

Original languageEnglish
Pages (from-to)538-544
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume121
Issue number2
DOIs
Publication statusPublished - Jun 15 1984

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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