The effects of temperature on the biophysical properties of optic nerve F-fibres
Autor: | Dafydd O. Plant, Sophie Knott, Mark D. Baker, Ella M. B. Richards, Azab Khan, Lavinia J. Austerschmidt |
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Rok vydání: | 2020 |
Předmět: |
Male
0301 basic medicine Multiple Sclerosis Physiology Biophysics Q10 Action Potentials lcsh:Medicine Article Membrane Potentials 03 medical and health sciences chemistry.chemical_compound Nerve Fibers 0302 clinical medicine Chlorides Potassium Channel Blockers Extracellular medicine Animals Solute Carrier Family 12 Member 2 Channel blocker Rats Wistar lcsh:Science Ions Membrane potential Multidisciplinary Tetraethylammonium Chemistry Sodium lcsh:R Temperature Optic Nerve Transporter Axons Rats 030104 developmental biology Optic nerve lcsh:Q 030217 neurology & neurosurgery Bumetanide Neuroscience medicine.drug |
Zdroj: | Scientific Reports, Vol 10, Iss 1, Pp 1-12 (2020) Scientific Reports |
ISSN: | 2045-2322 |
DOI: | 10.1038/s41598-020-69728-y |
Popis: | In multiple sclerosis, exacerbation of symptoms with rising body temperature is associated with impulse conduction failure. The mechanism is not fully understood. Remarkably, normal optic nerve axons also show temperature dependent effects, with a fall in excitability with warming. Here we show two properties of optic nerve axons, accommodation and inward rectification (Ih), respond to temperature changes in a manner consistent with a temperature dependent membrane potential. As we could find no evidence for the functional expression of KV7.2 in the axons, using the K+ channel blocker tetraethylammonium ions, we suggest this may explain the membrane potential lability. In order to understand how the axonal membrane potential may show temperature dependence, we have developed a hypothesis involving the electroneutral movement of Na+ ions across the axon membrane, that increases with increasing temperature with an appropriate Q10. Part, but probably not all, of the electroneutral Na+ movement is eliminated by removing extracellular Cl− or exposure to bumetanide, consistent with the involvement of the transporter NKCC1. Numerical simulation suggests a change in membrane potential of − 15–20 mV mimics altering temperature between room and physiological in the largest axons. |
Databáze: | OpenAIRE |
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