Department of Anesthesiology

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Dynamin phosphorylation controls optimization of endocytosis for brief action potential bursts.

TitleDynamin phosphorylation controls optimization of endocytosis for brief action potential bursts.
Publication TypeJournal Article
Year of Publication2013
AuthorsArmbruster M, Messa M, Ferguson SM, De Camilli P, Ryan TA
JournalElife
Volume2
Paginatione00845
Date Published2013
ISSN2050-084X
Abstract

Modulation of synaptic vesicle retrieval is considered to be potentially important in steady-state synaptic performance. Here we show that at physiological temperature endocytosis kinetics at hippocampal and cortical nerve terminals show a bi-phasic dependence on electrical activity. Endocytosis accelerates for the first 15-25 APs during bursts of action potential firing, after which it slows with increasing burst length creating an optimum stimulus for this kinetic parameter. We show that activity-dependent acceleration is only prominent at physiological temperature and that the mechanism of this modulation is based on the dephosphorylation of dynamin 1. Nerve terminals in which dynamin 1 and 3 have been replaced with dynamin 1 harboring dephospho- or phospho-mimetic mutations in the proline-rich domain eliminate the acceleration phase by either setting endocytosis at an accelerated state or a decelerated state, respectively. DOI:http://dx.doi.org/10.7554/eLife.00845.001.

DOI10.7554/eLife.00845
Alternate JournalElife
PubMed ID23908769
PubMed Central IDPMC3728620
Grant ListP30 DA018343 / DA / NIDA NIH HHS / United States