Journal article
Synaptophysin sustains presynaptic performance by preserving vesicular synaptobrevin-II levels
AC Kokotos, CB Harper, JRK Marland, KJ Smillie, MA Cousin, SL Gordon
Journal of Neurochemistry | WILEY | Published : 2019
DOI: 10.1111/jnc.14797
Abstract
The two most abundant molecules on synaptic vesicles (SVs) are synaptophysin and synaptobrevin-II (sybII). SybII is essential for SV fusion, whereas synaptophysin is proposed to control the trafficking of sybII after SV fusion and its retrieval during endocytosis. Despite controlling key aspects of sybII packaging into SVs, the absence of synaptophysin results in negligible effects on neurotransmission. We hypothesised that this apparent absence of effect may be because of the abundance of sybII on SVs, with the impact of inefficient sybII retrieval only revealed during periods of repeated SV turnover. To test this hypothesis, we subjected primary cultures of synaptophysin knockout neurons t..
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Funding Acknowledgements
This work was supported by a grant from the Biotechnology and Biological Sciences Research Council to MAC (BB/L019329/1) and a grant and Career Development Fellowship from The National Health and Medical Research Council (NHMRC) of Australia to SLG (GNT1085483). ACK was supported by a Marie-Curie Initial Training Network award (Project number 289581 -NPlast) to MAC. JRKM and KJS were supported by a grant from the Medical Research Council (G1002117). The Florey Institute of Neuroscience and Mental Health acknowledges the strong support from the Victorian Government and in particular the funding from the Operational Infrastructure Support Grant. We thank members of the Gordon and Cousin labs for helpful discussions. The authors declare no conflict of interest.