| Annotated protein: | Cannabinoid receptor 1 (CB-R) (CB1) (Brain-type cannabinoid receptor). Gene symbol: CNR1. Taxonomy: Mus musculus (Mouse). Uniprot ID: P47746 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ CNR1 |
| Ontology domain: | Biological Process |
| SynGO term: | retrograde trans-synaptic signaling by endocannabinoid (GO:0098921) |
| Synapse type(s): | hippocampus, GABAergic hippocampus, glutamatergic |
| Annotated paper: | Wilson RI, et al. "Presynaptic specificity of endocannabinoid signaling in the hippocampus" Neuron. 2001 Aug 16;31(3):453-62 PMID:11516401 |
| Figure(s): | Figure 1C,D |
| Annotation description: | Figure 1C,D: Depolarization of CA1 postsynaptic pyramidal neurons mobilizes endocannabinoids, which retrogradely activate presynaptic CB1 receptors, transiently decreasing GABAergic inhibitory neurotransmission (depolarization-induced suppression of inhibition or DSI) or glutamatergic excitatory neurotransmission (depolarization-induced suppression of excitation or DSE). DSI is lost in CB1 knockout mice (Figure 1C,D). Additionally, DSE is lost in CB1 knockout mice (Figure 8A of Ohno-Shosaku, T. et al (2002) J Neurosci, 22(10), 3864-3872). Figure 3: In addition, evidence is shown that presynaptic N-Type Ca2+ channels are required for endocannabinoid signaling. DSI is occluded by a specific antagonist of N-type channels, ω-conotoxin GVIA, indicating a presynaptic requirement for N-type calcium channels in the regulation of GABAergic transmission by cannabinoids. Conversely, blocking P/Q-type channels results in increased DSI (removes a component of GABA release that is insensitive to DSI and therefore modulation of N-type calcium channels by cannabinoids is now very relevant). |
| 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): | 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: | Depolarization-induced production of endocannabinoids activates presynaptic CB1 receptors in glutamatergic neurons, which inhibits glutamate release in a process called depolarization-induced suppression of excitation (DSE). DSE is lost in CB1 knockout mice (Figure 8A). @ PMID:12019305 |
| SynGO annotation ID: | 1066 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |