ArticleThe Journal of physiology2006
Bidirectional modulation of GABAergic transmission by cholecystokinin in hippocampal dentate gyrus granule cells of juvenile rats.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 54 citations in OpenAlex.
- Medial preoptic CCKAR mediates anxiety and aggression induced by chronic emotional stress in male mice.National science review · 2025Article
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- Restoring Synaptic Function: How Intranasal Delivery of 3D-Cultured hUSSC Exosomes Improve Learning and Memory Deficits in Alzheimer's Disease.Molecular neurobiology · 2024Article
- Neuropeptides Modulate Local Astrocytes to Regulate Adult Hippocampal Neural Stem Cells.Neuron · 2020Article
- Cholecystokinin Switches the Plasticity of GABA Synapses in the Dorsomedial Hypothalamus via Astrocytic ATP Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Cholecystokinin selectively activates short axon cells to enhance inhibition of olfactory bulb output neurons.The Journal of physiology · 2018Article
- Postsynaptic Depolarization Enhances GABA Drive to Dorsomedial Hypothalamic Neurons through Somatodendritic Cholecystokinin Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Dopaminergic modulation of GABAergic transmission in the entorhinal cortex: concerted roles of α1 adrenoreceptors, inward rectifier K⁺, and T-type Ca²⁺ channels.Cerebral cortex (New York, N.Y. : 1991) · 2014Article
- Neuropeptides as targets for the development of anticonvulsant drugs.Molecular neurobiology · 2014Review
- Article
- Vasopressin facilitates GABAergic transmission in rat hippocampus via activation of V(1A) receptors.Neuropharmacology · 2012Article
- Phospholipase C not protein kinase C is required for the activation of TRPC5 channels by cholecystokinin.European journal of pharmacology · 2012Article
- Requirement of phospholipase C and protein kinase C in cholecystokinin-mediated facilitation of NMDA channel function and anxiety-like behavior.Hippocampus · 2012Article
- Activation of group II metabotropic glutamate receptors inhibits glutamatergic transmission in the rat entorhinal cortex via reduction of glutamate release probability.Cerebral cortex (New York, N.Y. : 1991) · 2012Article
- Increased cholecystokinin labeling in the hippocampus of a mouse model of epilepsy maps to spines and glutamatergic terminals.Neuroscience · 2012Article
- Cholecystokinin facilitates neuronal excitability in the entorhinal cortex via activation of TRPC-like channels.Journal of neurophysiology · 2011Article
- Cell-type-specific CCK2 receptor signaling underlies the cholecystokinin-mediated selective excitation of hippocampal parvalbumin-positive fast-spiking basket cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Requirement for CB1 but not GABAB receptors in the cholecystokinin mediated inhibition of GABA release from cholecystokinin expressing basket cells.The Journal of physiology · 2011Article
- Brain expression and song regulation of the cholecystokinin gene in the zebra finch (Taeniopygia guttata).The Journal of comparative neurology · 2011Article
- Cholecystokinin: a multi-functional molecular switch of neuronal circuits.Developmental neurobiology · 2011Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cholecystokinin (CCK) interacts with two types of G protein-coupled receptors in the brain: CCK-A and CCK-B receptors. Both CCK and CCK-B receptors are widely distributed in the hippocampal formation, but the functions of CCK there have been poorly understood. In the present study, we initially examined the effects of CCK on GABA(A) receptor-mediated synaptic transmission in the hippocampal formation and then explored the underlying cellular mechanisms by focusing on the dentate gyrus region, where the highest levels of CCK-binding sites have been detected. Our results indicate that activation of CCK-B receptors initially and transiently increased spontaneous IPSC (sIPSC) frequency, followed by a persistent reduction. The effects of CCK were more evident in juvenile rats, suggesting that they are developmentally regulated. Cholecystokinin failed to modulate the miniature IPSCs recorded in the presence of TTX and the amplitude of the evoked IPSCs, but produced a transient increase followed by a reduction in action potential firing frequency recorded from GABAergic interneurons, suggesting that CCK acts by modulating the excitability of the interneurons to regulate GABA release. Cholecystokinin reduced the amplitude of the after-hyperpolarization of the action potentials, and application of paxilline or charybdotoxin considerably reduced CCK-mediated modulation of sIPSC frequency, suggesting that the effects of CCK are related to the inhibition of Ca(2+)-activated K(+) currents (I(K(Ca))). The effects of CCK were independent of the functions of phospholipase C, intracellular Ca(2+) release, protein kinase C or phospholipase A(2), suggesting a direct coupling between the G proteins of CCK-B receptors and I(K(Ca)). Our results provide a novel mechanism underlying CCK-mediated modulation of GABA release.
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Registered trials
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.