Vti1a Identifies a Vesicle Pool that Preferentially Recycles at Rest and Maintains Spontaneous Neurotransmission

Denise M O Ramirez, Mikhail Khvotchev, Brent Trauterman, Ege T. Kavalali

Research output: Contribution to journalArticle

105 Scopus citations

Abstract

Recent studies suggest that synaptic vesicles (SVs) giving rise to spontaneous neurotransmission are distinct from those that carry out evoked release. However, the molecular basis of this dichotomy remains unclear. Here, we focused on two noncanonical SNARE molecules, Vps10p-tail-interactor-1a (vti1a) and VAMP7, previously shown to reside on SVs. Using simultaneous multicolor imaging at individual synapses, we could show that compared to the more abundant vesicular SNARE synaptobrevin2, both vti1a and VAMP7 were reluctantly mobilized during activity. Vti1a, but not VAMP7, showed robust trafficking under resting conditions that could be partly matched by synaptobrevin2. Furthermore, loss of vti1a function selectively reduced high-frequency spontaneous neurotransmitter release detected postsynaptically. Expression of a truncated version of vti1a augmented spontaneous release more than full-length vti1a, suggesting that an autoinhibitory process regulates vti1a function. Taken together, these results support the premise that in its native form vti1a selectively maintains spontaneous neurotransmitter release. Recent studies suggest that synaptic vesicles giving rise to spontaneous neurotransmission are distinct from those that carry out evoked release. Ramirez etal. address the role of the synaptic vesicle-associated SNARE protein vti1a and demonstrate a selective role for this protein in spontaneous neurotransmitter release.

Original languageEnglish (US)
Pages (from-to)121-134
Number of pages14
JournalNeuron
Volume73
Issue number1
DOIs
StatePublished - Jan 12 2012

ASJC Scopus subject areas

  • Neuroscience(all)

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