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Related Concept Videos

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...
Action Potential01:14

Action Potential

Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...
Propagation of Action Potentials01:23

Propagation of Action Potentials

The propagation of an action potential refers to the process by which a nerve impulse, or "action potential," travels along a neuron.
Neurons (nerve cells) have a resting membrane potential, with a slightly negative charge inside compared to outside. This is maintained by ion channels, such as sodium (Na+) and potassium (K+) channels, which control the flow of ions. When a stimulus, like a touch or a signal from another neuron, triggers the neuron, sodium channels open, allowing sodium ions to...
Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
Action Potentials01:41

Action Potentials

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Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure
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Activity-dependent conduction failure: molecular insights.

Susanna B Park1, Cindy S-Y Lin, David Burke

  • 1Prince of Wales Clinical School, University of New South Wales, Sydney, Australia.

Journal of the Peripheral Nervous System : JPNS
|October 19, 2011
PubMed
Summary
This summary is machine-generated.

Weakness and fatigue in neurological disorders stem from axonal membrane dysfunction. Activity-dependent conduction failure, assessed by impulse trains, reveals disease severity in neuropathies and ALS.

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Area of Science:

  • Neuroscience
  • Neurology
  • Physiology

Background:

  • Weakness and fatigue are common, quality-of-life-limiting symptoms in neurological disorders.
  • Axonal membrane dysfunction, involving channels and pumps, underlies these symptoms.
  • Conduction block in motor axons contributes to weakness, fatigue, and aberrant nerve activity.

Purpose of the Study:

  • To critically appraise techniques for assessing activity-dependent conduction failure in neurological disorders.
  • To explore the physiological mechanisms of activity-dependent hyperpolarization.
  • To focus on demyelinating neuropathies (MMN, CIDP) and ALS.

Main Methods:

  • Review of physiological mechanisms of axonal impulse conduction.
  • Analysis of how activity impacts axonal membrane potential and ion channel function.
  • Evaluation of neurophysiological techniques, particularly impulse train analysis, for assessing conduction failure.

Main Results:

  • Conduction failure can be precipitated by activity in conditions like multifocal motor neuropathy (MMN) and chronic inflammatory demyelinating polyneuropathy (CIDP).
  • Conventional neurophysiological techniques may inadequately assess activity-dependent conduction failure.
  • Impulse train assessment is useful for determining the extent of conduction failure and resulting symptoms.

Conclusions:

  • Activity-dependent conduction failure is a key mechanism underlying weakness and fatigue in neurological diseases.
  • Advanced neurophysiological assessments are needed to adequately evaluate these symptoms.
  • Understanding these mechanisms is crucial for managing demyelinating neuropathies and ALS.