ArticleJournal of neurophysiology2011
Cholecystokinin facilitates neuronal excitability in the entorhinal cortex via activation of TRPC-like channels.
Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Trial
- Entorhinal Cholecystokinin in Alzheimer's Disease: Its Earliest Vulnerability and Rescue Effects Across Different Disease Stages in a Mouse Model.Cellular and molecular neurobiology · 2026Article
- TRPC4/5 inhibitors: Phase I results and proof of concept studies.European archives of psychiatry and clinical neuroscience · 2025Review
- Neuropeptidergic systems in psychiatric disorders.Frontiers in endocrinology · 2025Review
- Roles of KCNA2 in Neurological Diseases: from Physiology to Pathology.Molecular neurobiology · 2024Review
- Cortical VIPJournal of molecular neuroscience : MN · 2022Article
- Cholecystokinin-Mediated Neuromodulation of Anxiety and Schizophrenia: A "Dimmer-Switch" Hypothesis.Current neuropharmacology · 2021Review
- Role of Oxidative Stress and CaFrontiers in cell and developmental biology · 2021Review
- Contribution of TRPC Channels in Neuronal Excitotoxicity Associated With Neurodegenerative Disease and Ischemic Stroke.Frontiers in cell and developmental biology · 2020Article
- Histamine facilitates GABAergic transmission in the rat entorhinal cortex: Roles of HHippocampus · 2017Article
- Neurotensinergic Excitation of Dentate Gyrus Granule Cells via Gαq-Coupled Inhibition of TASK-3 Channels.Cerebral cortex (New York, N.Y. : 1991) · 2016Article
- Neurotensinergic augmentation of glutamate release at the perforant path-granule cell synapse in rat dentate gyrus: Roles of L-Type Ca²⁺ channels, calmodulin and myosin light-chain kinase.Neuropharmacology · 2015Article
- Acute Treatment with a Novel TRPC4/C5 Channel Inhibitor Produces Antidepressant and Anxiolytic-Like Effects in Mice.PloS one · 2015Article
- Human cerebrospinal fluid increases the excitability of pyramidal neurons in the in vitro brain slice.The Journal of physiology · 2015Article
- RNA-seq analysis of broiler liver transcriptome reveals novel responses to high ambient temperature.BMC genomics · 2014Article
- 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
- Activation of neurotensin receptor 1 facilitates neuronal excitability and spatial learning and memory in the entorhinal cortex: beneficial actions in an Alzheimer's disease model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Transient and sustained afterdepolarizations in accessory olfactory bulb mitral cells are mediated by distinct mechanisms that are differentially regulated by neuromodulators.Frontiers in cellular neuroscience · 2014Article
- Corticotropin-releasing factor facilitates epileptiform activity in the entorhinal cortex: roles of CRF2 receptors and PKA pathway.PloS one · 2014Article
- Persistent sodium current drives conditional pacemaking in CA1 pyramidal neurons under muscarinic stimulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
Cholecystokinin (CCK) is one of the most abundant neuropeptides in the brain, where it interacts with two G protein-coupled receptors (CCK-1 and CCK-2). Activation of both CCK receptors increases the activity of PLC, resulting in increases in intracellular calcium ion (Ca(2+)) release and activation of PKC. Whereas high density of CCK receptors has been detected in the superficial layers of the entorhinal cortex (EC), the functions of CCK in this brain region have not been determined. Here, we studied the effects of CCK on neuronal excitability of layer III pyramidal neurons in the EC. Our results showed that CCK remarkably increased the firing frequency of action potentials (APs). The effects of CCK on neuronal excitability were mediated via activation of CCK-2 receptors and required the functions of G proteins and PLC. However, CCK-mediated facilitation of neuronal excitability was independent of inositol trisphosphate receptors and PKC. CCK facilitated neuronal excitability by activating a cationic channel to generate membrane depolarization. The effects of CCK were suppressed by the generic, nonselective cationic channel blockers, 2-aminoethyldiphenyl borate and flufenamic acid, but potentiated by gadolinium ion and lanthanum ion at 100 μM. Depletion of extracellular Ca(2+) also counteracted CCK-induced increases in AC firing frequency. Moreover, CCK-induced enhancement of neuronal excitability was inhibited significantly by intracellular application of the antibody to transient receptor potential channel 5 (TRPC5), suggesting the involvement of TRPC5 channels. Our results provide a cellular and molecular mechanism to help explain the functions of CCK in vivo.
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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.