| Annotated protein: | Inositol 1,4,5-trisphosphate receptor type 1 (IP3 receptor isoform 1) (IP3R 1) (InsP3R1) (Inositol 1,4,5-trisphosphate-binding protein P400) (Protein PCD-6) (Purkinje cell protein 1) (Type 1 inositol 1,4,5-trisphosphate receptor) (Type 1 InsP3 receptor). Gene symbol: ITPR1. Taxonomy: Mus musculus (Mouse). Uniprot ID: P11881 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ ITPR1 |
| Ontology domain: | Biological Process |
| SynGO term: | inositol 1,4,5-trisphosphate receptor activity involved in regulation of postsynaptic cytosolic calcium levels (GO:0098695) |
| Synapse type(s): | Schaffer collateral synapse (CA3->CA1) |
| Annotated paper: | Nishiyama M, et al. "Calcium stores regulate the polarity and input specificity of synaptic modification" Nature. 2000 Nov 30;408(6812):584-8 PMID:11117745 |
| Figure(s): | Fig 4, Fig 5 |
| Annotation description: | To study synaptic plasticity, the authors correlated pre- and postsynaptic activation using a train of stimuli (16s, 5 Hz) delivered to one Schaffer collateral/commissural input that was paired with a postsynaptic injection of a spike-inducing depolarizing current. Two conditions were studied: (1) when the onset of EPSPs was about 20 ms after postsynaptic spiking, the EPSC amplitude of both stimulated (homosynaptic) and non-stimulated (heterosynaptic) inputs showed a persistent reduction following the correlated activation (LTD protocol) and (2) when the onset of EPSPs was about 5 ms before postsynaptic spiking, the EPSC amplitude of the homosynaptic input showed a persistent increase in amplitude whereas the one of the heterosynaptic input was not affected (LTP protocol). Functional blockade of IP3R1 by postsynaptic loading of a monoclonal antibody against IP3R1 or genetic deletion of IP3R1 using IP3R1-deficient mice impacted both conditions: when studying LTD (1) lacking IP3R1 function led to a conversion of homosynaptic LTD to LTP and eliminated heterosynaptic LTD. When studying LTP (2) a significant enhancement of homosynaptic LTP was observed, resulting in even higher potentiation. Therefore, IP3R1 presents a role in regulating Ca2+ release from internal stores in the postsynaptic neuron, which can control polarity and magnitude of postsynaptic plasticity. |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) Antagonist / agonist |
| Evidence tracking, Experiment Assay: | Electrophysiology (generic) |
| Annotator(s): | Ryan J. Farrell (ORCID:0000-0003-4022-8707) Ghazaleh Ashrafi (ORCID:0000-0001-7480-0826) Camila Pulido (ORCID:0000-0002-5648-066X) Jaime de Juan-Sanz (ORCID:0000-0002-1212-5623) Timothy Ryan (ORCID:0000-0003-2533-9548) |
| Lab: | Department of Biochemistry, Weill Cornell Medicine, New York, NY 10065, USA |
| Additional literature: | Generation of IP3R1-deficient mice used @ PMID:8538767 |
| SynGO annotation ID: | 159 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |