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Nat Neurosci. 2009 Aug;12(8):1003-1010. doi: 10.1038/nn.2355. Epub 2009 Jul 26.

Ca(2+) and calmodulin initiate all forms of endocytosis during depolarization at a nerve terminal.

Author information

1
National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA.
2
Department of Pulmonary Medicine, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA.
#
Contributed equally

Erratum in

  • Nat Neurosci. 2010 May;13(5):649. Dosage error in article text.

Abstract

Although endocytosis maintains synaptic transmission, how endocytosis is initiated is unclear. We found that calcium influx initiated all forms of endocytosis at a single nerve terminal in rodents, including clathrin-dependent slow endocytosis, bulk endocytosis, rapid endocytosis and endocytosis overshoot (excess endocytosis), with each being evoked with a correspondingly higher calcium threshold. As calcium influx increased, endocytosis gradually switched from very slow endocytosis to slow endocytosis to bulk endocytosis to rapid endocytosis and to endocytosis overshoot. The calcium-induced endocytosis rate increase was a result of the speeding up of membrane invagination and fission. Pharmacological experiments suggested that the calcium sensor mediating these forms of endocytosis is calmodulin. In addition to its role in recycling vesicles, calcium/calmodulin-initiated endocytosis facilitated vesicle mobilization to the readily releasable pool, probably by clearing fused vesicle membrane at release sites. Our findings provide a unifying mechanism for the initiation of various forms of endocytosis that are critical in maintaining exocytosis.

PMID:
19633667
PMCID:
PMC4887276
DOI:
10.1038/nn.2355
[Indexed for MEDLINE]
Free PMC Article

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