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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Bolshakov, V. Y. Hammer, R. E. Siegelbaum, S. A. Mcmahon, H. T. Südhof, T. C. Janz, R. |
| Description | Author Affiliation: McMahon HT ( Howard Hughes Medical Institute, The University of Texas Southwestern Medical School, Dallas 75235, USA.); |
| Abstract | Synaptophysin (syp I) is a synaptic vesicle membrane protein that constitutes approximately 7% of the total vesicle protein. Multiple lines of evidence implicate syp I in a number of nerve terminal functions. To test these, we have disrupted the murine Syp I gene. Mutant mice lacking syp I were viable and fertile. No changes in the structure and protein composition of the mutant brains were observed except for a decrease in synaptobrevin/VAMP II. Synaptic transmission was normal with no detectable changes in synaptic plasticity or the probability of release. Our data demonstrate that one of the major synaptic vesicle membrane proteins is not essential for synaptic transmission, suggesting that its function is either redundant or that it has a more subtle function not apparent in the assays used. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 10 |
| Volume Number | 93 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 1996-07-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Neurotransmitter Agents Secretion Synaptic Vesicles Physiology Synaptophysin Animals Calcium Metabolism Chromosome Mapping DNA Primers Genetics Electrophysiology Mice Mice, Knockout Molecular Sequence Data Neuronal Plasticity Phenotype Synaptic Transmission Deficiency Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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