| Annotated protein: | Synaptophysin (BM89 antigen) (Major synaptic vesicle protein p38). Gene symbol: SYP. Taxonomy: Mus musculus (Mouse). Uniprot ID: Q62277 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ SYP |
| Ontology domain: | Biological Process |
| SynGO term: | modulation of chemical synaptic transmission (GO:0050804) |
| Synapse type(s): | Schaffer collateral synapse (CA3->CA1) |
| Annotated paper: | Janz R, et al. "Essential roles in synaptic plasticity for synaptogyrin I and synaptophysin I" Neuron. 1999 Nov;24(3):687-700 PMID:10595519 |
| Figure(s): | Fig. 5C; Fig. 6C, Fig. 7 C-D |
| Annotation description: | In this paper, the authors demonstrate impairment of short-term and long-term plasticity in synaptogyrin/synaptophysin double knockout (DKO) mice (Fig. 5C; Fig. 6C, Fig. 7 C-D): No changes in basal synaptic transmission were observed: CA3->CA1 EPSPs and paired-pulse facilitation (PPF) at all interpulse intervals, providing no evidence for a role of these proteins in exocytosis (but see PMID: 31090538) However, the study reveals significant impairment of short-term plasticity in DKO (Fig. 5C). Furthermore, posttetanic potentiation (PTP) in DKO and synaptogyrin 1 single KO is reduced by 50% (Fig. 6C), suggesting involvement in physiological PTP induction. Moreover, long-term plasticity (LTP) in response to tetanic field stimulation of Shaeffer collateral pathway is significantly reduced (Fig. 7). In order to exclude LTP impairment as a secondary consequence of reduced PTP, LTP is measured in voltage-pairing protocol, which confirms the observation. Thus, this data suggests involvement of the two proteins, synaptophysin I and synaptogyrin 1, in modulation of chemical synaptic transmission by an unknown mechanism. |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Whole-cell patch clamp |
| Annotator(s): | Matthijs Verhage (ORCID:0000-0002-2514-0216) |
| Lab: | Department of Functional Genomics, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands |
| Additional literature: | First report on mice lacking synaptophysin I gene. @ PMID:8581936 Fig. 2, 3 and 4: In order to explore possible effects of synaptophysin I deletion, the authors performed series of electrophysiological recordings. EPSCs displayed no difference between mutant and wt mice. In addition, no changes in few forms of synaptic plasticity were observed - paired-pulse facilitation, frequency facilitation during repetitive stimulation and long-term potentiation (fig. 2). Quantal size analysis of synaptic transmission revealed no changes in synaptic function (Fig. 3). These results suggest no effect of synaptophysin deletion on Ca2+-triggered transmitter release. Additionally, McMahon et al tested effect of gene deletion on spontaneous release events (fig. 4) and failed to observe any differences between mutant and wt mice. Overall, this data suggests no effect of synaptophysin on Ca-dependent or Ca-independent neurotransmitter release. @ PMID:8643476 |
| SynGO annotation ID: | 4958 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |