ArticleThe Journal of physiology2012
M-type potassium channels modulate Schaffer collateral-CA1 glutamatergic synaptic transmission.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
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- Loose-patch recordings reveal differential Kv7-dependent effects on spontaneous excitatory activity in control and epileptic CA1.Frontiers in neurology · 2026Article
- Status epilepticus: Updates on mechanisms and treatments.Epilepsia open · 2025Review
- Advances in magnetic field approaches for non-invasive targeting neuromodulation.Frontiers in human neuroscience · 2025Review
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- Glycolytic lactate production supports status epilepticus in experimental animals.Annals of clinical and translational neurology · 2023Article
- Single Neuron Modeling Identifies Potassium Channel Modulation as Potential Target for Repetitive Head Impacts.Neuroinformatics · 2023Article
- Glycolysis regulates neuronal excitability via lactate receptor, HCA1R.Brain : a journal of neurology · 2023Article
- Evidence for Dual Activation ofInternational journal of molecular sciences · 2022Article
- Acetylcholine Boosts Dendritic NMDA Spikes in a CA3 Pyramidal Neuron Model.Neuroscience · 2022Article
- Inhibition of Matrix Metalloproteinase 9 Activity Promotes Synaptogenesis in the Hippocampus.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- Difluoroboron β-diketonate polylactic acid oxygen nanosensors for intracellular neuronal imaging.Scientific reports · 2021Article
- The M-current works in tandem with the persistent sodium current to set the speed of locomotion.PLoS biology · 2020Article
- Chronic Stress Induces Maladaptive Behaviors by Activating Corticotropin-Releasing Hormone Signaling in the Mouse Oval Bed Nucleus of the Stria Terminalis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- The Role of KFrontiers in physiology · 2020Review
- The dual role of KCNQ/M channels upon OGD or OGD/R insults in cultured cortical neurons of mice: Timing is crucial in targeting M-channels against ischemic injur ies.Journal of cellular physiology · 2019Article
- Mechanisms of status epilepticus: α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor hypothesis.Epilepsia · 2018Article
- Functional up-regulation of the M-current by retigabine contrasts hyperexcitability and excitotoxicity on rat hypoglossal motoneurons.The Journal of physiology · 2018Article
- A novel therapeutic approach for treatment of catamenial epilepsy.Neurobiology of disease · 2018Article
- Pharmacological modulation of the voltage-gated neuronal Kv7/KCNQ/M-channel alters the intrinsic excitability and synaptic responses of pyramidal neurons in rat prefrontal cortex slices.Acta pharmacologica Sinica · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have suggested that muscarinic receptor activation modulates glutamatergic transmission. M-type potassium channels mediate the effects of muscarinic activation in the hippocampus, and it has been proposed that they modulate glutamatergic synaptic transmission. We tested whether M1 muscarinic receptor activation enhances glutamatergic synaptic transmission via the inhibition of the M-type potassium channels that are present in Schaffer collateral axons and terminals. Miniature excitatory postsynaptic currents (mEPSCs) were recorded from CA1 pyramidal neurons. The M1 receptor agonist, NcN-A-343, increased the frequency of mEPSCs, but did not alter their amplitude. The M-channel blocker XE991 and its analogue linopirdine also increased the frequency of mEPSCs. Flupirtine, which opens M-channels, had the opposite effect. XE991 did not enhance mEPSCs frequency in a calcium-free external medium. Blocking P/Q- and N-type calcium channels abolished the effect of XE991 on mEPSCs. These data suggested that the inhibition of M-channels increases presynaptic calcium-dependent glutamate release in CA1 pyramidal neurons. The effects of these agents on the membrane potentials of presynaptic CA3 pyramidal neurons were studied using current clamp recordings; activation of M1 receptors and blocking M-channels depolarized neurons and increased burst firing. The input resistance of CA3 neurons was increased by the application of McN-A-343 and XE991; these effects were consistent with the closure of M-channels. Muscarinic activation inhibits M-channels in CA3 pyramidal neurons and its efferents – Schaffer collateral, which causes the depolarization, activates voltage-gated calcium channels, and ultimately elevates the intracellular calcium concentration to increase the release of glutamate on CA1 pyramidal neurons.
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