ArticleThe Journal of physiology2006
Metabotropic glutamate receptor subtype 1 regulates sodium currents in rat neocortical pyramidal neurons.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Neuromodulation of voltage-gated sodium channels by Gβ1γ2 subunits: Implications for GNB1-linked encephalopathy.Neurobiology of disease · 2025Article
- Article
- A hypothesis concerning distinct schemes of olfactory activation evoked by perceived versus nonperceived input.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Cinacalcet inhibition of neuronal action potentials preferentially targets the fast inactivated state of voltage-gated sodium channels.Frontiers in physiology · 2022Article
- Strong G-Protein-Mediated Inhibition of Sodium Channels.Cell reports · 2018Article
- Does Epileptiform Activity Represent a Failure of Neuromodulation to Control Central Pattern Generator-Like Neocortical Behavior?Frontiers in neural circuits · 2017Article
- Differential ability of the dorsal and ventral rat hippocampus to exhibit group I metabotropic glutamate receptor-dependent synaptic and intrinsic plasticity.Brain and neuroscience advances · 2017Article
- Increased Persistent Sodium Current Causes Neuronal Hyperexcitability in the Entorhinal Cortex of Fmr1 Knockout Mice.Cell reports · 2016Article
- Postsynaptic mGluR5 promotes evoked AMPAR-mediated synaptic transmission onto neocortical layer 2/3 pyramidal neurons during development.Journal of neurophysiology · 2015Article
- Activation of group I metabotropic glutamate receptors enhances persistent sodium current and rhythmic bursting in main olfactory bulb external tufted cells.Journal of neurophysiology · 2014Article
- Phenytoin inhibits the persistent sodium current in neocortical neurons by modifying its inactivation properties.PloS one · 2013Article
- Glutamate modulates the firing rate in oculomotor nucleus motoneurons as a function of the recruitment threshold current.The Journal of physiology · 2012Article
- Dendritic Signaling in Inhibitory Interneurons: Local Tuning via Group I Metabotropic Glutamate Receptors.Frontiers in physiology · 2012Article
- The role of hyperpolarization-activated cationic current in spike-time precision and intrinsic resonance in cortical neurons in vitro.The Journal of physiology · 2011Article
- Activation of group I metabotropic glutamate receptors modulates locomotor-related motoneuron output in mice.Journal of neurophysiology · 2011Article
- Presynaptic action potential waveform determines cortical synaptic latency.The Journal of physiology · 2011Article
- Spike-timing dependent plasticity beyond synapse - pre- and post-synaptic plasticity of intrinsic neuronal excitability.Frontiers in synaptic neuroscience · 2010Article
- Activation of mGluR5 induces spike afterdepolarization and enhanced excitability in medium spiny neurons of the nucleus accumbens by modulating persistent Na+ currents.The Journal of physiology · 2009Article
- Action potential initiation and propagation: upstream influences on neurotransmission.Neuroscience · 2009Review
- Downregulation of dendritic I(h) in CA1 pyramidal neurons after LTP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain sodium channels (NaChs) are regulated by various neurotransmitters such as acetylcholine, serotonin and dopamine. However, it is not known whether NaCh activity is regulated by glutamate, the principal brain neurotransmitter. We show here that activation of metabotropic glutamate receptor (mGluR) subtype 1 regulates fast transient (I(NaT)) and persistent Na(+) currents (I(NaP)) in cortical pyramidal neurons. A selective agonist of group I mGluR, (S)-3,5-dihydroxyphenylglycine (DHPG), reduced action potential amplitude and decreased I(NaT). This reduction was blocked when DHPG was applied in the presence of selective mGluR1 antagonists. The DHPG-induced reduction of the current was accompanied by a shift of both the inactivation curve of I(NaT) and the activation curve of I(NaP). These effects were dependent on the activation of PKC. The respective role of these two regulatory processes on neuronal excitability was determined by simulating transient and persistent Na(+) conductances (G(NaT) and G(NaP)) with fast dynamic-clamp techniques. The facilitated activation of G(NaP) increased excitability near the threshold, but, when combined with the down-regulation of G(NaT), repetitive firing was strongly decreased. Consistent with this finding, the mGluR1 antagonist LY367385 increased neuronal excitability when glutamatergic synaptic activity was stimulated with high external K(+). We conclude that mGluR1-dependent regulation of Na(+) current depresses neuronal excitability, which thus might constitute a novel mechanism of homeostatic regulation acting during intense glutamatergic synaptic activity.
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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.