Conditional deletions of epilepsy-associated KCNQ2 and KCNQ3 channels from cerebral cortex cause differential effects on neuronal excitability
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Neonatal Seizures: Impact on Neurodevelopmental OutcomesM-current preservation contributes to anticonvulsant effects of valproic acid.Molecular underpinnings of ventral surface chemoreceptor function: focus on KCNQ channelsRetigabine, a Kv7.2/Kv7.3-Channel Opener, Attenuates Drug-Induced Seizures in Knock-In Mice Harboring Kcnq2 MutationsDV21 decreases excitability of cortical pyramidal neurons and acts in epilepsy.Activation of m1 muscarinic acetylcholine receptor induces surface transport of KCNQ channels through a CRMP-2-mediated pathway.Potent KCNQ2/3-specific channel activator suppresses in vivo epileptic activity and prevents the development of tinnitusKV7 Channels Regulate Firing during Synaptic Integration in GABAergic Striatal Neurons.Retigabine holds KV7 channels open and stabilizes the resting potential.Involvement of cortical fast-spiking parvalbumin-positive basket cells in epilepsy.Epilepsy-Associated KCNQ2 Channels Regulate Multiple Intrinsic Properties of Layer 2/3 Pyramidal NeuronsPotassium Channels in Epilepsy.Ion channel regulation by β-secretase BACE1 - enzymatic and non-enzymatic effects beyond Alzheimer's disease.KCNQ Potassium Channels Modulate Sensitivity of Skin Down-hair (D-hair) Mechanoreceptors.Modulation of Kv7 channels and excitability in the brain.Cortical KCNQ2/3 channels; insights from knockout mice.Rapid and efficient CRISPR/Cas9 gene inactivation in human neurons during human pluripotent stem cell differentiation and direct reprogramming.XE991 and Linopirdine Are State-Dependent Inhibitors for Kv7/KCNQ Channels that Favor Activated Single Subunits.Abnormal γ-aminobutyric acid neurotransmission in a Kcnq2 model of early onset epilepsy.Coordinated Expression of Two Types of Low-Threshold K+ Channels Establishes Unique Single Spiking of Mauthner Cells among Segmentally Homologous Neurons in the Zebrafish Hindbrain.A possible link between KCNQ2- and STXBP1-related encephalopathies: STXBP1 reduces the inhibitory impact of syntaxin-1A on M current.Genetic perturbations suggest a role of the resting potential in regulating the expression of the ion channels of the KCNA and HCN families in octopus cells of the ventral cochlear nucleus.
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Conditional deletions of epilepsy-associated KCNQ2 and KCNQ3 channels from cerebral cortex cause differential effects on neuronal excitability
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article científic
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artigo científico
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bilimsel makale
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scientific article published on April 2014
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name
Conditional deletions of epile ...... fects on neuronal excitability
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Conditional deletions of epile ...... ects on neuronal excitability.
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Conditional deletions of epile ...... fects on neuronal excitability
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Conditional deletions of epile ...... ects on neuronal excitability.
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Conditional deletions of epile ...... fects on neuronal excitability
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Conditional deletions of epile ...... ects on neuronal excitability.
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Conditional deletions of epile ...... fects on neuronal excitability
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Anastasios V Tzingounis
Joseph J LoTurco
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10.1523/JNEUROSCI.3919-13.2014
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2014-04-01T00:00:00Z