Arachidonic acid potentiates exocytosis and allows neuronal SNARE complex to interact with Munc18a

Catherine F. Latham, Shona L. Osborne, Max J. Cryle, Frederic A. Meunier

Research output: Contribution to journalArticleResearchpeer-review

57 Citations (Scopus)

Abstract

Neuronal communication relies on the fusion of neurotransmitter-containing vesicles with the neuronal plasma membrane. Recent genetic studies have highlighted the critical role played by polyunsaturated fatty acids in neurotransmission, however, there is little information available about which fatty acids act on exocytosis and, more importantly, by what mechanism. We have used permeabilized chromaffin cells to screen various fatty acids of the n-3 and n-6 series for their acute effects on exocytosis. We have demonstrated that an n-6 series polyunsaturated fatty acid, arachidonic acid, potentiates secretion from intact neurosecretory cells regardless of the secretagogue used. We have shown that arachidonic acid dose dependently increases soluble NSF attachment protein receptor complex formation in chromaffin cells and bovine cortical brain extracts and that a non-hydrolysable analogue of arachidonic acid causes a similar increase in SNARE complex formation. This prompted us to examine the effect of arachidonic acid on SNARE protein interactions with Munc18a, a protein known to prevent Syntaxin1a engagement into the SNARE complex in vitro. In the presence of arachidonic acid, we show that Munc18a can interact with the neuronal SNARE complex in a dose-dependent manner. We further demonstrate that arachidonic acid directly interacts with Syntaxin1a.

Original languageEnglish
Pages (from-to)1543-1554
Number of pages12
JournalJournal of Neurochemistry
Volume100
Issue number6
DOIs
Publication statusPublished - Mar 2007
Externally publishedYes

Keywords

  • Arachidonic acid
  • Exocytosis
  • Munc18a
  • Soluble NSF attachment protein receptor
  • Syntaxin1a

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