ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2023
A Novel CCK Receptor GPR173 Mediates Potentiation of GABAergic Inhibition.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- New insights into SREB orphan receptor roles in the ovary, using comparative transcriptomics across 3 fishes.Endocrinology · 2026Article
- AAV-mediated GPR173 gene therapy attenuates long-term refractory epilepsy by enhancing synaptic GABAActa pharmacologica Sinica · 2026Article
- International Union of Basic and Clinical Pharmacology. CXXII. Applying an objective evaluation to the status of class A orphan G protein-coupled receptors.Pharmacological reviews · 2026Review
- Stress-responsive nucleus accumbens dopamine D2 receptor-expressing neurons modulate cocaine-induced behavioral sensitization.Frontiers in cellular neuroscience · 2026Article
- Discovery of a β-arrestin-biased CCKBR agonist that blocks CCKBR-dependent long-term potentiation.Nature communications · 2025Article
- Upregulation of CCK3R leading to the suppression of chronic seizures.Translational psychiatry · 2025Article
- Cholecystokinin: Clinical aspects of the new biology.Journal of internal medicine · 2025Review
- Cholecystokinin-expressing GABA neurons elicit long-term potentiation in the cortical inhibitory synapses and attenuate sound-shock associative memory.Scientific reports · 2025Article
- Immunolocalization and quantification of the phoenixin and GPR173 in the gastrointestinal tract of Holstein-Friesian bulls.BMC veterinary research · 2025Article
- Spatial and quantitative gene expression analysis of SREB receptors in the gonads of green-spotted pufferfish (Dichotomyctere nigroviridis).General and comparative endocrinology · 2025Article
- Goldfish phoenixin: (I) structural characterization, tissue distribution, and novel function as a feedforward signal for feeding-induced food intake in fish model.Frontiers in endocrinology · 2025Article
- Cholecystokinin-expressing interneurons mediated inhibitory transmission and plasticity in basolateral amygdala modulate stress-induced anxiety-like behaviors in mice.Neurobiology of stress · 2024Article
- Basolateral amygdala parvalbumin and cholecystokinin-expressing GABAergic neurons modulate depressive and anxiety-like behaviors.Translational psychiatry · 2024Article
- Characterizing dysregulations via cell-cell communications in Alzheimer's brains using single-cell transcriptomes.BMC neuroscience · 2024Article
- Potentiated GABAergic neuronal activities in the basolateral amygdala alleviate stress-induced depressive behaviors.CNS neuroscience & therapeutics · 2024Article
- Article
- Characterizing the SREB G protein-coupled receptor family in fish: Brain gene expression and genomic differences in upstream transcription factor binding sites.Comparative biochemistry and physiology. Part A, Molecular & integrative physiology · 2023Article
- Neuronal diversity of neuropeptide signaling, including galanin, in the mouse locus coeruleus.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Advances in the Electrophysiological Recordings of Long-Term Potentiation.International journal of molecular sciences · 2023Review
- Cholecystokinin neurotransmission in the central nervous system: Insights into its role in health and disease.BioFactors (Oxford, England)Review
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholecystokinin (CCK) enables excitatory circuit long-term potentiation (LTP). Here, we investigated its involvement in the enhancement of inhibitory synapses. Activation of GABA neurons suppressed neuronal responses in the neocortex to a forthcoming auditory stimulus in mice of both sexes. High-frequency laser stimulation (HFLS) of GABAergic neurons potentiated this suppression. HFLS of CCK interneurons could induce the LTP of their inhibition toward pyramidal neurons. This potentiation was abolished in CCK knock-out mice but intact in mice with both CCK1R and 2R knockout of both sexes. Next, we combined bioinformatics analysis, multiple unbiased cell-based assays, and histology examinations to identify a novel CCK receptor, GPR173. We propose GPR173 as CCK3R, which mediates the relationship between cortical CCK interneuron signaling and inhibitory LTP in the mice of either sex. Thus, GPR173 might represent a promising therapeutic target for brain disorders related to excitation and inhibition imbalance in the cortex.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.