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Related Concept Videos

Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

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Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several...
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Antiepileptic Drugs: Potassium Channel Activators01:20

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Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
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Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

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Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
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The Role of Ion Channels in Neuronal Computation01:19

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A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential....
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Excitatory and Inhibitory Effects of Neurotransmitters01:29

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When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
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Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

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Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
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Patch Clamp and Perfusion Techniques for Studying Ion Channels Expressed in Xenopus oocytes
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Kv7 Channels and Excitability Disorders.

Frederick Jones1, Nikita Gamper2,3, Haixia Gao4

  • 1Faculty of Biological Sciences, University of Leeds, Leeds, UK.

Handbook of Experimental Pharmacology
|April 16, 2021
PubMed
Summary

Kv7 (KCNQ) potassium channels control cell excitability and are crucial for neuronal and cardiac function. Deficiencies cause disorders like epilepsy and arrhythmias, highlighting their therapeutic potential.

Keywords:
ChannelopathyEpilepsyKCNQKv7 channelM currentPain

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Related Experiment Videos

Last Updated: Nov 9, 2025

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Area of Science:

  • Molecular Biology
  • Neuroscience
  • Cardiology

Background:

  • Kv7 channels (Kv7.1-Kv7.5 or KCNQ1-5) are voltage-gated ion channels vital for excitable cells.
  • They regulate neuronal M current and cardiac IKs, controlling cellular activity.
  • Genetic defects in KCNQ genes lead to human excitability disorders.

Purpose of the Study:

  • To review the biophysical properties and tissue expression of Kv7 channels.
  • To discuss structural insights and roles in diseases.
  • To explore therapeutic targeting strategies for Kv7 channels.

Main Methods:

  • Literature review of biophysical properties.
  • Analysis of tissue expression profiles.
  • Examination of structure-function relationships and disease associations.

Main Results:

  • Kv7 channels possess unique biophysical traits enabling control of cell excitability.
  • They are implicated in neurological, cardiovascular, and other pathologies.
  • Understanding their structure and function is key to therapeutic development.

Conclusions:

  • Kv7 channels are critical regulators of cellular excitability.
  • Their dysfunction underlies significant human diseases.
  • Targeting Kv7 channels offers promising therapeutic avenues for various conditions.