| Annotated protein: | Neuronal calcium sensor 1 (NCS-1) (Frequenin homolog) (Frequenin-like protein) (Frequenin-like ubiquitous protein). Gene symbol: NCS1. Taxonomy: Rattus norvegicus (Rat). Uniprot ID: P62168 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ NCS1 |
| Ontology domain: | Biological Process |
| SynGO term: | regulation of synaptic vesicle exocytosis (GO:2000300) |
| Synapse type(s): | hippocampus, glutamatergic |
| Annotated paper: | Sippy T, et al. "Acute changes in short-term plasticity at synapses with elevated levels of neuronal calcium sensor-1" Nat Neurosci. 2003 Oct;6(10):1031-8 PMID:12947410 |
| Figure(s): | Figure 1, 2, 4 |
| Annotation description: | The paper studies the effect of NCS-1 overexpression in continental rat hippocampal neuron culture. Double patch clamp experiments in paired neurons allow the comparison between presynaptic-transfected and presynaptic-non-transfected neurons. The paper essentially shows that presynaptic overexpression of NCS-1 leads to a switch to activity-dependent facilitation, from the otherwise observed depression in such cultures. Figure 1 demonstrates that in paired recordings from reciprocally connected neurons depression is seen in non-transfected presynaptic neurons whereas facilitation is seen at NCS-1 presynapticly transfected synapses. Figure 2 shows that even though the initial EPSC amplitudes are similar between controls and NCS-1-expressing neurons (Figure 2d), facilitation in seen in NCS-1-transfected synapses and depression in controls. This suggests that the effect of overexpression is on activity-dependent, rather than on basal transmitter release. Figure 4 shows that in NCS-1-transfected synapses continues facilitation is seen during high frequency stimulus trains. 20/01/2021 Dnyanada: P62168 (NCS1_RAT) was chosen on the basis of the biological system in which the experiment was conducted as the species of the overexpressed NCS-1 construct could not be retrieved. |
| Evidence tracking, Biological System: | Cultured neurons |
| Evidence tracking, Protein Targeting: | Over-expression |
| Evidence tracking, Experiment Assay: | Whole-cell patch clamp |
| Annotator(s): | Noa Lipstein (ORCID:0000-0002-0755-5899) Cordelia Imig (ORCID:0000-0001-7351-8706) Vincent O'connor (ORCID:0000-0003-3185-5709) Nils Brose (ORCID:0000-0003-0938-8534) |
| Lab: | Department of Molecular Neurobiology, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany |
| Additional literature: | Note: This data is copied from redundant and deleted ticket #725 The paper describes the NCS-1 knock-out mice for the first time and evaluates dopamine release to the nucleus accumbens. Figure 5 presents the analysis of dopamine release in acute slices containing the nucleus accumbens. The dopamine is measured by fast-scan cyclic voltammetry, while the presynaptic neurons are stimulated electrically 200 micrometer from the nucleus. The data shows a lower basal release and a substantially higher paired-pulse ratio in NCS-1 KO slices, indicating a lower initial release probability of dopamine release. The application of the D2 receptor antagonist Sulpiride increased dopamine release in both conditions. Figure 4 presents a sub-cellular fractionation of the striatum demonstrating identical expression levels of D2 receptor and the DAT transporter in the cytoplasmic and membrane fractions. This control suggests that the effects seen on dopamine release is due to and effect on the release machinery rather then on dopamine uptake or on differential negative-feedback to release by D2 signaling. While the molecular mechanism are not clearly studied here (e.g. - where in the SV cycle does NCS-1 exerts its effect), this paper is important because it demonstrates for the first time an effect of the deletion of NCS-1 on neurotransmitter release. @ PMID:26738968 |
| SynGO annotation ID: | 723 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |