Vesicles derived via AP-3-dependent recycling contribute to asynchronous release and influence information transfer.

TitleVesicles derived via AP-3-dependent recycling contribute to asynchronous release and influence information transfer.
Publication TypeJournal Article
Year of Publication2014
AuthorsEvstratova, A, Chamberland, S, Faundez, V, Toth, K
JournalNat Commun
Volume5
Pagination5530
Date Published2014 Nov 20
ISSN2041-1723
KeywordsAction Potentials, Adaptor Protein Complex 3, Adaptor Protein Complex beta Subunits, Animals, Endocytosis, Endosomes, Mice, Mice, Knockout, Synaptic Transmission, Synaptic Vesicles
Abstract

Action potentials trigger synchronous and asynchronous neurotransmitter release. Temporal properties of both types of release could be altered in an activity-dependent manner. While the effects of activity-dependent changes in synchronous release on postsynaptic signal integration have been studied, the contribution of asynchronous release to information transfer during natural stimulus patterns is unknown. Here we find that during trains of stimulations, asynchronous release contributes to the precision of action potential firing. Our data show that this form of release is selectively diminished in AP-3b2 KO animals, which lack functional neuronal AP-3, an adaptor protein regulating vesicle formation from endosomes generated during bulk endocytosis. We find that in the absence of neuronal AP-3, asynchronous release is attenuated and the activity-dependent increase in the precision of action potential timing is compromised. Lack of asynchronous release decreases the capacity of synaptic information transfer and renders synaptic communication less reliable in response to natural stimulus patterns.

DOI10.1038/ncomms6530
Alternate JournalNat Commun
PubMed ID25410111
PubMed Central IDPMC4239664
Grant ListMOP-81142 / / Canadian Institutes of Health Research / Canada
R56 NS042599 / NS / NINDS NIH HHS / United States
NS42599 / NS / NINDS NIH HHS / United States
R01 NS042599 / NS / NINDS NIH HHS / United States
GM077569 / GM / NIGMS NIH HHS / United States
R01 GM077569 / GM / NIGMS NIH HHS / United States