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EMBO J. 2011 Sep 16;30(24):4955-69. doi: 10.1038/emboj.2011.339.

Proper synaptic vesicle formation and neuronal network activity critically rely on syndapin I.

Author information

1
Institute of Biochemistry I, Jena University Hospital-Friedrich Schiller University Jena, Jena, Germany.

Abstract

Synaptic transmission relies on effective and accurate compensatory endocytosis. F-BAR proteins may serve as membrane curvature sensors and/or inducers and thereby support membrane remodelling processes; yet, their in vivo functions urgently await disclosure. We demonstrate that the F-BAR protein syndapin I is crucial for proper brain function. Syndapin I knockout (KO) mice suffer from seizures, a phenotype consistent with excessive hippocampal network activity. Loss of syndapin I causes defects in presynaptic membrane trafficking processes, which are especially evident under high-capacity retrieval conditions, accumulation of endocytic intermediates, loss of synaptic vesicle (SV) size control, impaired activity-dependent SV retrieval and defective synaptic activity. Detailed molecular analyses demonstrate that syndapin I plays an important role in the recruitment of all dynamin isoforms, central players in vesicle fission reactions, to the membrane. Consistently, syndapin I KO mice share phenotypes with dynamin I KO mice, whereas their seizure phenotype is very reminiscent of fitful mice expressing a mutant dynamin. Thus, syndapin I acts as pivotal membrane anchoring factor for dynamins during regeneration of SVs.

PMID:
21926968
PMCID:
PMC3243622
DOI:
10.1038/emboj.2011.339
[Indexed for MEDLINE]
Free PMC Article

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