Neuroprotectant effects of iso-osmolar D-mannitol to prevent Pacific ciguatoxin-1 induced alterations in neuronal excitability: a comparison with other osmotic agents and free radical scavengers

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Neuroprotectant effects of iso-osmolar D-mannitol to prevent Pacific ciguatoxin-1 induced alterations in neuronal excitability : a comparison with other osmotic agents and free radical scavengers. / Birinyi-Strachan, Liesl C; Davies, Michael Jonathan; Lewis, Richard J; Nicholson, Graham M.

In: Neuropharmacology, Vol. 49, No. 5, 10.2005, p. 669-86.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Birinyi-Strachan, LC, Davies, MJ, Lewis, RJ & Nicholson, GM 2005, 'Neuroprotectant effects of iso-osmolar D-mannitol to prevent Pacific ciguatoxin-1 induced alterations in neuronal excitability: a comparison with other osmotic agents and free radical scavengers', Neuropharmacology, vol. 49, no. 5, pp. 669-86. https://doi.org/10.1016/j.neuropharm.2005.04.024

APA

Birinyi-Strachan, L. C., Davies, M. J., Lewis, R. J., & Nicholson, G. M. (2005). Neuroprotectant effects of iso-osmolar D-mannitol to prevent Pacific ciguatoxin-1 induced alterations in neuronal excitability: a comparison with other osmotic agents and free radical scavengers. Neuropharmacology, 49(5), 669-86. https://doi.org/10.1016/j.neuropharm.2005.04.024

Vancouver

Birinyi-Strachan LC, Davies MJ, Lewis RJ, Nicholson GM. Neuroprotectant effects of iso-osmolar D-mannitol to prevent Pacific ciguatoxin-1 induced alterations in neuronal excitability: a comparison with other osmotic agents and free radical scavengers. Neuropharmacology. 2005 Oct;49(5):669-86. https://doi.org/10.1016/j.neuropharm.2005.04.024

Author

Birinyi-Strachan, Liesl C ; Davies, Michael Jonathan ; Lewis, Richard J ; Nicholson, Graham M. / Neuroprotectant effects of iso-osmolar D-mannitol to prevent Pacific ciguatoxin-1 induced alterations in neuronal excitability : a comparison with other osmotic agents and free radical scavengers. In: Neuropharmacology. 2005 ; Vol. 49, No. 5. pp. 669-86.

Bibtex

@article{594f2639f02e42b6adff6ded7c55cde2,
title = "Neuroprotectant effects of iso-osmolar D-mannitol to prevent Pacific ciguatoxin-1 induced alterations in neuronal excitability: a comparison with other osmotic agents and free radical scavengers",
abstract = "The basis for the neuroprotectant effect of D-mannitol in reducing the sensory neurological disturbances seen in ciguatera poisoning, is unclear. Pacific ciguatoxin-1 (P-CTX-1), at a concentration 10 nM, caused a statistically significant swelling of rat sensory dorsal root ganglia (DRG) neurons that was reversed by hyperosmolar 50 mM D-mannitol. However, using electron paramagnetic resonance (EPR) spectroscopy, it was found that P-CTX-1 failed to generate hydroxyl free radicals at concentrations of toxin that caused profound effects on neuronal excitability. Whole-cell patch-clamp recordings from DRG neurons revealed that both hyper- and iso-osmolar 50 mM D-mannitol prevented the membrane depolarisation and repetitive firing of action potentials induced by P-CTX-1. In addition, both hyper- and iso-osmolar 50 mM D-mannitol prevented the hyperpolarising shift in steady-state inactivation and the rise in leakage current through tetrodotoxin (TTX)-sensitive Na(v) channels, as well as the increased rate of recovery from inactivation of TTX-resistant Na(v) channels induced by P-CTX-1. D-Mannitol also reduced, but did not prevent, the inhibition of peak TTX-sensitive and TTX-resistant I(Na) amplitude by P-CTX-1. Additional experiments using hyper- and iso-osmolar D-sorbitol, hyperosmolar sucrose and the free radical scavenging agents Trolox and L-ascorbic acid showed that these agents, unlike D-mannitol, failed to prevent the effects of P-CTX-1 on spike electrogenesis and Na(v) channel gating. These selective actions of D-mannitol indicate that it does not act purely as an osmotic agent to reduce swelling of nerves, but involves a more complex action dependent on the Na(v) channel subtype, possibly to alter or reduce toxin association.",
keywords = "Algorithms, Ascorbic Acid, Cell Size, Chromans, Ciguatoxins, Diuretics, Electron Spin Resonance Spectroscopy, Electrophysiology, Free Radical Scavengers, Ganglia, Spinal, Ion Channel Gating, Mannitol, Membrane Potentials, Neurons, Afferent, Neuroprotective Agents, Osmolar Concentration, Patch-Clamp Techniques, Sodium Channel Blockers, Sodium Channels, Sorbitol, Tetrodotoxin",
author = "Birinyi-Strachan, {Liesl C} and Davies, {Michael Jonathan} and Lewis, {Richard J} and Nicholson, {Graham M}",
year = "2005",
month = "10",
doi = "10.1016/j.neuropharm.2005.04.024",
language = "English",
volume = "49",
pages = "669--86",
journal = "Neuropharmacology",
issn = "0028-3908",
publisher = "Pergamon Press",
number = "5",

}

RIS

TY - JOUR

T1 - Neuroprotectant effects of iso-osmolar D-mannitol to prevent Pacific ciguatoxin-1 induced alterations in neuronal excitability

T2 - a comparison with other osmotic agents and free radical scavengers

AU - Birinyi-Strachan, Liesl C

AU - Davies, Michael Jonathan

AU - Lewis, Richard J

AU - Nicholson, Graham M

PY - 2005/10

Y1 - 2005/10

N2 - The basis for the neuroprotectant effect of D-mannitol in reducing the sensory neurological disturbances seen in ciguatera poisoning, is unclear. Pacific ciguatoxin-1 (P-CTX-1), at a concentration 10 nM, caused a statistically significant swelling of rat sensory dorsal root ganglia (DRG) neurons that was reversed by hyperosmolar 50 mM D-mannitol. However, using electron paramagnetic resonance (EPR) spectroscopy, it was found that P-CTX-1 failed to generate hydroxyl free radicals at concentrations of toxin that caused profound effects on neuronal excitability. Whole-cell patch-clamp recordings from DRG neurons revealed that both hyper- and iso-osmolar 50 mM D-mannitol prevented the membrane depolarisation and repetitive firing of action potentials induced by P-CTX-1. In addition, both hyper- and iso-osmolar 50 mM D-mannitol prevented the hyperpolarising shift in steady-state inactivation and the rise in leakage current through tetrodotoxin (TTX)-sensitive Na(v) channels, as well as the increased rate of recovery from inactivation of TTX-resistant Na(v) channels induced by P-CTX-1. D-Mannitol also reduced, but did not prevent, the inhibition of peak TTX-sensitive and TTX-resistant I(Na) amplitude by P-CTX-1. Additional experiments using hyper- and iso-osmolar D-sorbitol, hyperosmolar sucrose and the free radical scavenging agents Trolox and L-ascorbic acid showed that these agents, unlike D-mannitol, failed to prevent the effects of P-CTX-1 on spike electrogenesis and Na(v) channel gating. These selective actions of D-mannitol indicate that it does not act purely as an osmotic agent to reduce swelling of nerves, but involves a more complex action dependent on the Na(v) channel subtype, possibly to alter or reduce toxin association.

AB - The basis for the neuroprotectant effect of D-mannitol in reducing the sensory neurological disturbances seen in ciguatera poisoning, is unclear. Pacific ciguatoxin-1 (P-CTX-1), at a concentration 10 nM, caused a statistically significant swelling of rat sensory dorsal root ganglia (DRG) neurons that was reversed by hyperosmolar 50 mM D-mannitol. However, using electron paramagnetic resonance (EPR) spectroscopy, it was found that P-CTX-1 failed to generate hydroxyl free radicals at concentrations of toxin that caused profound effects on neuronal excitability. Whole-cell patch-clamp recordings from DRG neurons revealed that both hyper- and iso-osmolar 50 mM D-mannitol prevented the membrane depolarisation and repetitive firing of action potentials induced by P-CTX-1. In addition, both hyper- and iso-osmolar 50 mM D-mannitol prevented the hyperpolarising shift in steady-state inactivation and the rise in leakage current through tetrodotoxin (TTX)-sensitive Na(v) channels, as well as the increased rate of recovery from inactivation of TTX-resistant Na(v) channels induced by P-CTX-1. D-Mannitol also reduced, but did not prevent, the inhibition of peak TTX-sensitive and TTX-resistant I(Na) amplitude by P-CTX-1. Additional experiments using hyper- and iso-osmolar D-sorbitol, hyperosmolar sucrose and the free radical scavenging agents Trolox and L-ascorbic acid showed that these agents, unlike D-mannitol, failed to prevent the effects of P-CTX-1 on spike electrogenesis and Na(v) channel gating. These selective actions of D-mannitol indicate that it does not act purely as an osmotic agent to reduce swelling of nerves, but involves a more complex action dependent on the Na(v) channel subtype, possibly to alter or reduce toxin association.

KW - Algorithms

KW - Ascorbic Acid

KW - Cell Size

KW - Chromans

KW - Ciguatoxins

KW - Diuretics

KW - Electron Spin Resonance Spectroscopy

KW - Electrophysiology

KW - Free Radical Scavengers

KW - Ganglia, Spinal

KW - Ion Channel Gating

KW - Mannitol

KW - Membrane Potentials

KW - Neurons, Afferent

KW - Neuroprotective Agents

KW - Osmolar Concentration

KW - Patch-Clamp Techniques

KW - Sodium Channel Blockers

KW - Sodium Channels

KW - Sorbitol

KW - Tetrodotoxin

U2 - 10.1016/j.neuropharm.2005.04.024

DO - 10.1016/j.neuropharm.2005.04.024

M3 - Journal article

C2 - 15950247

VL - 49

SP - 669

EP - 686

JO - Neuropharmacology

JF - Neuropharmacology

SN - 0028-3908

IS - 5

ER -

ID: 129672003