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Related Concept Videos

Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

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 types of...
Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

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 types of...
The Role of Ion Channels in Neuronal Computation01:19

The Role of Ion Channels in Neuronal Computation

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.
Mechanically-gated Ion Channels01:12

Mechanically-gated Ion Channels

Mechanically-gated ion channels are proteins found in eukaryotic and prokaryotic cell membranes that open in response to mechanical stress. Tension, compression, swelling, and shear stress can alter the conformation of the protein, opening a transmembrane channel that allows the passage of ions for signal transmission. In eukaryotes, mechanically-gated channels are distributed in several regions like the neurons, lungs, skin, bladder, and heart, where they play critical roles in numerous...
Mechanically-gated Ion Channels01:12

Mechanically-gated Ion Channels

Mechanically-gated ion channels are proteins found in eukaryotic and prokaryotic cell membranes that open in response to mechanical stress. Tension, compression, swelling, and shear stress can alter the conformation of the protein, opening a transmembrane channel that allows the passage of ions for signal transmission. In eukaryotes, mechanically-gated channels are distributed in several regions like the neurons, lungs, skin, bladder, and heart, where they play critical roles in numerous...
Non-gated Ion Channels01:24

Non-gated Ion Channels

Ion channels are specialized proteins on the plasma membrane that allow charged ions to pass down their electrochemical gradient. Their main function is to maintain the membrane potential which is critical for cell viability. These channels are either gated or non-gated and can transport more than a thousand ions within milliseconds for the cellular event to occur.
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.

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Modeling Biological Membranes with Circuit Boards and Measuring Electrical Signals in Axons: Student Laboratory Exercises
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Physiological interactions between Na(v)1.7 and Na(v)1.8 sodium channels: a computer simulation study.

Jin-Sung Choi1, Stephen G Waxman

  • 1College of Pharmacy, Catholic University of Korea, Bucheon, Gyeonggi-Do, South Korea.

Journal of Neurophysiology
|September 24, 2011
PubMed
Summary
This summary is machine-generated.

Computer simulations reveal how sodium channel Na(v)1.8 and Na(v)1.7 expression levels tune dorsal root ganglion neuron excitability. Changes in these sodium channels significantly impact action potential generation and firing frequency.

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Area of Science:

  • Neuroscience
  • Computational Biology
  • Ion Channel Physiology

Background:

  • Dorsal root ganglion (DRG) neurons are crucial for pain and sensory perception.
  • Sodium channels Na(v)1.7 and Na(v)1.8 play significant roles in DRG neuron function and excitability.
  • The interplay between Na(v)1.7 and Na(v)1.8 expression levels and their functional consequences remains incompletely understood.

Purpose of the Study:

  • To investigate the functional impact of varying expression levels of sodium channel Na(v)1.8 on DRG neurons co-expressing Na(v)1.7.
  • To elucidate how altered expression of sodium channel Na(v)1.7 affects DRG neurons that also express Na(v)1.8.
  • To understand the regulatory mechanisms tuning DRG neuron excitability through sodium channel expression.

Main Methods:

  • Utilized computational simulations to model DRG neuron function.
  • Analyzed the effects of varying Na(v)1.7 and Na(v)1.8 expression levels on neuronal electrical properties.
  • Examined parameters including current threshold, action potential threshold, subthreshold oscillations, and firing frequency.

Main Results:

  • Increased Na(v)1.7 expression reduced current threshold and modulated action potential threshold dependence on membrane potential.
  • Na(v)1.7 presence in Na(v)1.8 expressing cells enhanced subthreshold oscillations and repetitive firing frequency.
  • Na(v)1.8 expression at significant levels eliminated/reversed current threshold dependence on membrane potential.
  • Na(v)1.8 alone supported subthreshold oscillations and was essential for overshooting action potentials, prolonging them.
  • Higher Na(v)1.8 levels reduced Na(v)1.7 current due to inactivation accumulation.

Conclusions:

  • Altered expression levels of Na(v)1.7 and Na(v)1.8 significantly influence DRG neuron excitability.
  • These sodium channels exhibit complex interactions affecting neuronal firing properties.
  • Expression level changes of Na(v)1.7 and Na(v)1.8 serve as a regulatory mechanism for tuning DRG neuron excitability.