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Related Concept Videos

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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.
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Related Experiment Video

Updated: Apr 16, 2026

Recording Temperature-induced Neuronal Activity through Monitoring Calcium Changes in the Olfactory Bulb of Xenopus laevis
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Acute temperature sensitivity in optic nerve axons explained by an electrogenic membrane potential.

Tom A Coates1, Oscar Woolnough1, Joseph M Masters1

  • 1Neuroscience and Trauma Centre, Blizard Institute, Barts and the London School of Medicine, Queen Mary University of London, 4 Newark Street, London, E12AT, UK.

Pflugers Archiv : European Journal of Physiology
|March 1, 2015
PubMed
Summary

Mammalian optic nerve axons show temperature-dependent membrane potential, unlike squid. Warming enhances potential via a temperature-sensitive sodium cycle involving Na+/K+ ATPase and NKCC1 transporter.

Keywords:
BumetanideMembrane potentialNKCC1Na+/K+-ATPaseOptic nerveOuabainRecovery cycle

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Area of Science:

  • Neuroscience
  • Cellular Physiology

Background:

  • Classical studies on squid axons indicate resting membrane potential is temperature-independent.
  • This contrasts with observations in other excitable tissues, suggesting potential differences in temperature sensitivity.

Purpose of the Study:

  • To investigate the temperature dependence of resting membrane potential and refractory period in mammalian optic nerve axons.
  • To elucidate the underlying ionic mechanisms contributing to observed temperature effects.

Main Methods:

  • Electrophysiological recordings from mammalian optic nerve axons at varying temperatures.
  • Application of pharmacological agents like ouabain and bumetanide to probe specific ion transporters.

Main Results:

  • Resting membrane potential and refractory period duration in mammalian optic nerve axons are significantly temperature-sensitive.
  • Warming enhances membrane potential, an effect diminished by ouabain, suggesting a role for Na+/K+ ATPase.
  • Blockade of NKCC1 transporter with bumetanide increased refractoriness, implicating it in sodium influx.

Conclusions:

  • Mammalian optic nerve axons exhibit temperature-dependent membrane potential, contrary to squid axon models.
  • A temperature-dependent transmembrane sodium cycle, involving Na+/K+ ATPase and NKCC1, contributes significantly to membrane potential and nerve excitability.