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Activity-dependent alternative splicing increases persistent sodium current and promotes seizure.

Wei-Hsiang Lin1, Cengiz Günay, Richard Marley

  • 1Faculty of Life Sciences, University of Manchester, Manchester M13 9PL, United Kingdom.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|May 25, 2012
PubMed
Summary

Altered splicing of voltage-gated sodium channels (Na(v)) in Drosophila larvae contributes to seizure-like behavior. Increased inclusion of exon L enhances persistent sodium current (I(Nap)), promoting neuronal hyperexcitability and seizures.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Voltage-gated sodium channels (Na(v)) are crucial for neuronal excitability.
  • Alternative splicing of Na(v) transcripts can alter channel function.
  • The contribution of altered Na(v) splicing to epilepsy is not fully understood.

Purpose of the Study:

  • To investigate the role of alternative splicing of the Drosophila Na(v) (paralytic, DmNa(v)) in seizure-like behavior.
  • To identify the specific splice variants and regulatory mechanisms involved in activity-dependent splicing.
  • To determine if increased persistent sodium current (I(Nap)) can promote seizure phenotypes.

Main Methods:

  • Analysis of DmNa(v) splicing patterns in wild-type and seizure mutant Drosophila larvae.
  • Pharmacological manipulation of synaptic activity using phenytoin, GABA, and picrotoxin.
  • Investigation of the role of the RNA-binding protein Pasilla.
  • Computational modeling of channel activity and neuronal excitability.

Main Results:

  • Seizure mutants exhibit increased inclusion of exon L in DmNa(v) transcripts, leading to enhanced I(Nap).
  • Synaptic activity levels regulate DmNa(v) splicing, with increased excitation promoting exon L inclusion.
  • The RNA-binding protein Pasilla is required for this activity-dependent splicing.
  • Computational models confirm that increased I(Nap) potentiates neuronal excitability and seizure phenotype.

Conclusions:

  • Altered splicing of DmNa(v), specifically increased exon L inclusion, contributes to seizure-like behavior in Drosophila.
  • A self-reinforcing cycle exists where increased synaptic excitation promotes exon L inclusion, further increasing neuronal excitability.
  • This study provides a model for how altered Na(v) splicing may contribute to epilepsy.