Spinal Cord Research Help
AboutCategoriesLatest ResearchContact
Subscribe
Spinal Cord Research Help

Making Spinal Cord Injury (SCI) Research Accessible to Everyone. Simplified summaries of the latest research, designed for patients, caregivers and anybody who's interested.

Quick Links

  • Home
  • About
  • Categories
  • Latest Research
  • Disclaimer

Contact

  • Contact Us
© 2025 Spinal Cord Research Help

All rights reserved.

  1. Home
  2. Research
  3. Neurology
  4. Dynamics of sodium channel Nav 1.5 expression in astrocytes in mouse models of multiple sclerosis

Dynamics of sodium channel Nav 1.5 expression in astrocytes in mouse models of multiple sclerosis

Neuroreport, 2014 · DOI: 10.1097/WNR.0000000000000249 · Published: October 22, 2014

NeurologyGenetics

Simple Explanation

Astrocytes, brain cells, react to injury in multiple sclerosis (MS). While they don't usually have Nav1.5 sodium channels, these appear in MS lesions. The study explores how Nav1.5 expression changes over time in mice with MS-like conditions. The study examined mice with conditions similar to MS, observing astrocytes to see if Nav1.5 expression correlated with disease severity or relapse/remission phases. Results showed Nav1.5 increased in astrocytes with worsening disease. In mice experiencing relapses and remissions, Nav1.5 levels in astrocytes rose during relapses and decreased during remissions. This suggests Nav1.5 plays a role in how astrocytes respond to inflammation in the brain.

Study Duration
9-59 days
Participants
18 C57BL/6 and 20 Biozzi mice
Evidence Level
Not specified

Key Findings

  • 1
    Nav1.5 is upregulated in astrocytes in situ in a temporal manner that correlates with disease severity in both monophasic and chronic-relapsing EAE.
  • 2
    In chronic-relapsing EAE, Nav1.5 expression is upregulated during relapses and subsequently attenuated during periods of remission.
  • 3
    Low level of Nav1.5 expression in astrocytes of control animals suggests that Nav1.5 upregulation is part of the biological response of astrocytes to CNS insult.

Research Summary

The study investigated the expression of Nav1.5 in astrocytes in mouse models of multiple sclerosis (MS), specifically monophasic and chronic-relapsing experimental autoimmune encephalomyelitis (EAE). Results showed that Nav1.5 upregulation in astrocytes correlated with the severity of the disease in both EAE models. Furthermore, in chronic-relapsing EAE, Nav1.5 expression was upregulated during relapse phases and attenuated during remission phases, indicating a dynamic response of astrocytes to neuroinflammation.

Practical Implications

Therapeutic Target

Nav1.5 may be a potential therapeutic target to modulate reactive astrogliosis in vivo.

Understanding MS Progression

Understanding the temporal dynamics of Nav1.5 expression can provide insights into the role of astrocytes in the progression of MS.

Sodium Channel Blockade

Attenuation of reactive astrogliosis could contribute to the improved outcomes seen with sodium channel blockade.

Study Limitations

  • 1
    Study conducted on mouse models, may not fully translate to human MS.
  • 2
    The mechanisms underlying Nav1.5 regulation in astrocytes were not fully elucidated.
  • 3
    Further research is needed to validate Nav1.5 as a therapeutic target.

Your Feedback

Was this summary helpful?

Back to Neurology