| First Author | Koch D | Year | 2011 |
| Journal | EMBO J | Volume | 30 |
| Issue | 24 | Pages | 4955-69 |
| PubMed ID | 21926968 | Mgi Jnum | J:180017 |
| Mgi Id | MGI:5304995 | Doi | 10.1038/emboj.2011.339 |
| Citation | Koch D, et al. (2011) Proper synaptic vesicle formation and neuronal network activity critically rely on syndapin I. EMBO J 30(24):4955-69 |
| abstractText | 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. |
