Nitric oxide stimulates Ca2+-independent synaptic vesicle release

Mollie K. Meffert, Brett A. Premack, Howard Schulman

Research output: Contribution to journalArticlepeer-review

Abstract

A new fluorescence method using the dye FM1-43 was used to examine exocytotic release from hippocampal synaptosomes. Nitric oxide caused a marked transient stimulation of vesicle release. Several structurally unrelated nitric oxide donors, sodium nitroprusside, S-nitroso-N-acetylpenicillamine, 3-morpholino-sydnonimine, and acidified sodium nitrite, were effective. Release stimulated by nitric oxide and KCI were comparable in time course, using both the fluorescence assay and [3H]l-glutamate to monitor neurotransmitter release. Activation of guanylyl cyclase was not responsible for nitric oxide-stimulated release. Unlike release stimulated by KCl or A23187, nitric oxide-stimulated release was found to be independent of a rise in intrasynaptosomal Ca2+. Indo-1/AM measurements indicated that nitric oxide actually decreased intracellular Ca2+, and the Ca2+ channel blocker Cd2+ did not affect nitric oxide-stimulated vesicle release. Nitric oxide does, however, appear to act on the Ca2+-sensitive pool of vesicles. Nitric oxide may be the first physiological mediator that induces vesicle exocytosis without raising Ca2+ and may provide an interesting new tool for the study of molecules involved in vesicle exocytosis.

Original languageEnglish (US)
Pages (from-to)1235-1244
Number of pages10
JournalNeuron
Volume12
Issue number6
DOIs
StatePublished - Jun 1994
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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