ArticlePflugers Archiv : European journal of physiology2015
Acute temperature sensitivity in optic nerve axons explained by an electrogenic membrane potential.
Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Application of near infra-red laser light increases current threshold in optic nerve consistent with increased NaPflugers Archiv : European journal of physiology · 2024Article
- Changing the firing threshold for normal optic nerve axons by the application of infra-red laser light.Scientific reports · 2021Article
- Experience with the COVID-19 AstraZeneca vaccination in people with multiple sclerosis.Multiple sclerosis and related disorders · 2021Article
- Hypothermic neuroprotection during reperfusion following exposure to aglycemia in central white matter is mediated by acidification.Physiological reports · 2019Article
- Diuretic-sensitive electroneutral NaThe Journal of physiology · 2017Article
- Some do not like it hot.The Journal of physiology · 2017Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Classical work in squid axon reports resting membrane potential is independent of temperature, but our findings suggest that this is not the case for axons in mammalian optic nerve. Refractory period duration changes over 10 times between 37 °C and room temperature, and afterpotential polarity is also acutely temperature sensitive, inconsistent with changes in temperature impacting nerve function only through altered rates of ion channel gating kinetics. Our evidence suggests that the membrane potential is enhanced by warming, an effect reduced by exposure to ouabain. The temperature dependence can be explained if axonal Na(+)/K(+) ATPase continuously expels Na(+) ions that enter axons largely electroneutrally, thereby adding a substantial electrogenic component to the membrane potential. Block of the Na(+) transporter NKCC1 with bumetanide increases refractoriness, like depolarization, indicating that this is a probable route by which Na(+) enters, raising the expectation that the rate of electroneutral Na(+) influx increases with temperature and suggesting a temperature-dependent transmembrane Na(+) cycle that contributes to membrane potential.
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Registered trials
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