| Annotated protein: | Calbindin (Calbindin D28) (D-28K) (PCD-29) (Spot 35 protein) (Vitamin D-dependent calcium-binding protein, avian-type). Gene symbol: CALB1. Taxonomy: Mus musculus (Mouse). Uniprot ID: P12658 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ CALB1 |
| Ontology domain: | Biological Process |
| SynGO term: | calcium ion binding involved in regulation of presynaptic cytosolic calcium levels (GO:0099534) |
| Synapse type(s): | neocortex, GABAergic hippocampus, glutamatergic Mossy fiber synapse (DG->CA3) |
| Annotated paper: | Blatow M, et al. "Ca2+ buffer saturation underlies paired pulse facilitation in calbindin-D28k-containing terminals" Neuron. 2003 Apr 10;38(1):79-88 PMID:12691666 |
| Figure(s): | Figure 1, 2 and 3A,B |
| Annotation description: | The paper elegantly characterized the role of calbindin as a Ca2+ buffer at the presynaptic compartment of multipolar bursting interneurons in the mouse neocortex. Paired whole cell recordings of presynaptic interneurons synapsing on pyramidal cells in layer 2/3 were made. In WT pairs, paired-pulse facilitation of the IPSPs is seen when two depolarizations are given with a 10 Hz frequency (Fig 2A left). After a long recordings, the first IPSC is increased in amplitude and the PPF is reduced (Figure 2A right and 2B left). In calbindin KOs, the first IPSC amplitude is increased already at the start of the recordings, the initial PPF is reduced (2C left and 2B right), and there is no change following long recordings (2B left). These data suggest that in WT cells, a Ca2+ buffer in the presynapse limits the size of the first IPSC and leads to a strong PPF. During the long recordings the buffer is washed out into the recording electrode, the first IPSC amplitudes increases in size and the PPF is reduced. Figure 2C (right) shows that calbindin loading in the presynaptic compartment of the knockout interneuron reduces the amplitude of first IPSP and restores facilitation. There is little effect of the loading in WT synapses. Figure 3 A and B show similar effects on the initial IPSC amplitude and on the PPR when loading a WT terminal where the endogenous Ca2+ buffer has been washed out with the fast Ca2+-buffer BAPTA. Taken together, these data demonstrate a role for calbindin as a Ca2+ buffer regulating presynaptic Ca2+ concentrations, basal release probability and short-term synaptic plasticity at the presynapse of interneurons. In figure 5 and 6 similar effects are documented in CA3 mossy fiber calbindin KO synapses. |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Electrophysiology (generic) |
| 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 |
| SynGO annotation ID: | 885 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |