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Related Concept Videos

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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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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Ligand-gated Ion Channels01:19

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Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...
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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
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Published on: July 19, 2019

Astrocytes within multiple sclerosis lesions upregulate sodium channel Nav1.5.

Joel A Black1, Jia Newcombe, Stephen G Waxman

  • 1Neuroscience Research Centre (Bldg 34), VA Connecticut Healthcare System (127A), 950 Campbell Avenue, West Haven, CT 06516, USA.

Brain : a Journal of Neurology
|February 12, 2010
PubMed
Summary

Human astrocytes dynamically alter sodium channel Nav1.5 expression in response to central nervous system injury, particularly in multiple sclerosis lesions and around brain damage. This finding offers insights into reactive astrocyte function.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Immunology

Background:

  • Astrocytes are key players in the central nervous system's response to injury and neuroinflammation.
  • Rodent astrocytes exhibit dynamic voltage-gated sodium channel expression, shifting from tetrodotoxin-sensitive to tetrodotoxin-resistant types in reactive states.
  • The expression and regulation of sodium channels in human astrocytes, especially in reactive states, remain largely uncharacterized.

Purpose of the Study:

  • To investigate the expression patterns of voltage-gated sodium channels in human astrocytes.
  • To determine if sodium channel expression changes in reactive human astrocytes within central nervous system injury sites.
  • To explore the potential role of altered sodium channel expression in astrocyte-mediated ionic homeostasis following injury.

Main Methods:

  • Immunohistochemical analysis of human brain tissue samples.
  • Examination of astrocytes in normal control brain, multiple sclerosis lesions (active and chronic), and areas surrounding cerebrovascular accidents and brain tumors.
  • Assessment of the expression levels of specific sodium channel subtypes (Nav1.1, Nav1.2, Nav1.3, Nav1.5, Nav1.6) in astrocytes.

Main Results:

  • A significant and focal upregulation of sodium channel Nav1.5 was observed in reactive astrocytes at the borders and within active and chronic multiple sclerosis lesions.
  • Nav1.5 expression was minimal in astrocytes in macroscopically normal-appearing white matter of multiple sclerosis patients and in normal control brain tissue.
  • Nav1.5 was also highly expressed in astrocytes surrounding cerebrovascular accidents and brain tumors, while Nav1.1, Nav1.2, Nav1.3, and Nav1.6 showed limited or no significant upregulation in astrocytes across different injury types.

Conclusions:

  • This study demonstrates the expression of Nav1.5 in human astrocytes and reveals its dynamic regulation in reactive astrocytes.
  • The upregulated expression of Nav1.5 in astrocytes associated with central nervous system injury suggests a potential compensatory role.
  • This compensatory mechanism may support sodium/potassium pump-dependent ionic homeostasis in injured areas of the human central nervous system.