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A Simple and Inexpensive Method for Determining Cold Sensitivity and Adaptation in Mice
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Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents.

Sophia Kriegeskorte1, Raya Bott1, Martin Hampl2

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Investigating voltage-gated sodium channels (Nav) revealed temperature impacts channel gating. Lower temperatures exacerbate Nav1.3 and Nav1.7 mutation effects, influencing disease phenotypes.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Physiology

Background:

  • Voltage-gated sodium channels (Nav) are crucial for action potential generation in excitable tissues.
  • Mutations in Nav genes cause inherited channelopathies, some with temperature-sensitive phenotypes like pain syndromes.
  • Understanding temperature's role in channelopathies is limited due to studies often being at room temperature.

Purpose of the Study:

  • To investigate the temperature sensitivity of four Nav subtypes (Nav1.3, Nav1.5, Nav1.6, Nav1.7).
  • To examine the effects of temperature on two Nav1.7 mutations linked to inherited erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD).

Main Methods:

  • Utilized an automated patch clamp system to express and record from human embryonic kidney cells.
  • Tested Nav subtype and mutation function at three temperatures: 15°C, 25°C, and 35°C.

Main Results:

  • Increased temperature shifted the voltage dependence of activation to more hyperpolarized potentials across all tested Nav subtypes.
  • Nav1.3 showed significantly slowed inactivation at 15°C, leading to increased persistent current and potential cold-induced hyperexcitability.
  • The impaired fast inactivation in the Nav1.7/I1461T mutation (PEPD) was notably worsened at 15°C.

Conclusions:

  • Temperature significantly modulates Nav channel gating in a subtype-specific manner.
  • Cooling exacerbates the gating defects caused by specific Nav1.7 mutations, impacting cellular excitability.
  • Temperature should be considered a critical factor in understanding channelopathies and their disease phenotypes.