Excitability parameters and sensitivity to anemone toxin ATX-II in rat small diameter primary sensory neurones discriminated by Griffonia simplicifolia isolectin IB4
Sensory neurone subtypes (⤠25 μm apparent diameter) express a variety of Na + channels, where expression is linked to action potential duration, and associated with differential IB4-lectin binding. We hypothesized that sensitivity to ATX-II might also discriminate neurones and report that 1 μ m...
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| Published in | The Journal of physiology Vol. 588; no. 1; pp. 125 - 137 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
The Physiological Society
01.01.2010
Blackwell Publishing Ltd Wiley Subscription Services, Inc Blackwell Science Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3751 1469-7793 1469-7793 |
| DOI | 10.1113/jphysiol.2009.181107 |
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| Abstract | Sensory neurone subtypes (⤠25 μm apparent diameter) express a variety of Na + channels, where expression is linked to action potential duration, and associated with differential IB4-lectin binding. We
hypothesized that sensitivity to ATX-II might also discriminate neurones and report that 1 μ m has negligible or small effects on action potentials in IB4 +ve, but dramatically increased action potential duration in
IB4 âve, neurones. The toxin did not act on tetrodotoxin-resistant (TTX-r) Na V 1.8 currents; discrimination was based on tetrodotoxin-sensitive (TTX-s) Na + channel expression. We also explored the effects of varying the holding potential on current threshold, and the effect of
repetitive activation on action currents in IB4 +ve and âve neurones. IB4 +ve neurones became more excitable with depolarization
over the range â100 to â20 mV, but IB4 âve neurones exhibited peak excitability near â55 mV, and were inexcitable at â20 mV.
Eliciting action potentials at 2 Hz, we found that peak inward action current in IB4 +ve neurones was reduced, whereas changes
in the current amplitude were negligible in most IB4 âve neurones. Our findings are consistent with relatively toxin-insensitive
channels including Na V 1.7 being expressed in IB4 +ve neurones, whereas toxin sensitivity indicates that IB4 âve neurones may express Na V 1.1 or Na V 1.2, or both. The retention of excitability at low membrane potentials, and the responses to repetitive stimulation are explained
by the known preferential expression of Na V 1.8 in IB4 +ve neurones, and the reduction in action current in IB4 +ve neurones with repetitive stimulation supports a novel
hypothesis explaining the slowing of conduction velocity in C-fibres by the build-up of Na + channel inactivation. |
|---|---|
| AbstractList | Sensory neurone subtypes (⤠25 μm apparent diameter) express a variety of Na + channels, where expression is linked to action potential duration, and associated with differential IB4-lectin binding. We
hypothesized that sensitivity to ATX-II might also discriminate neurones and report that 1 μ m has negligible or small effects on action potentials in IB4 +ve, but dramatically increased action potential duration in
IB4 âve, neurones. The toxin did not act on tetrodotoxin-resistant (TTX-r) Na V 1.8 currents; discrimination was based on tetrodotoxin-sensitive (TTX-s) Na + channel expression. We also explored the effects of varying the holding potential on current threshold, and the effect of
repetitive activation on action currents in IB4 +ve and âve neurones. IB4 +ve neurones became more excitable with depolarization
over the range â100 to â20 mV, but IB4 âve neurones exhibited peak excitability near â55 mV, and were inexcitable at â20 mV.
Eliciting action potentials at 2 Hz, we found that peak inward action current in IB4 +ve neurones was reduced, whereas changes
in the current amplitude were negligible in most IB4 âve neurones. Our findings are consistent with relatively toxin-insensitive
channels including Na V 1.7 being expressed in IB4 +ve neurones, whereas toxin sensitivity indicates that IB4 âve neurones may express Na V 1.1 or Na V 1.2, or both. The retention of excitability at low membrane potentials, and the responses to repetitive stimulation are explained
by the known preferential expression of Na V 1.8 in IB4 +ve neurones, and the reduction in action current in IB4 +ve neurones with repetitive stimulation supports a novel
hypothesis explaining the slowing of conduction velocity in C-fibres by the build-up of Na + channel inactivation. Sensory neurone subtypes (≤ 25 µm apparent diameter) express a variety of Na+ channels, where expression is linked to action potential duration, and associated with differential IB4-lectin binding. We hypothesized that sensitivity to ATX-II might also discriminate neurones and report that 1 µm has negligible or small effects on action potentials in IB4 +ve, but dramatically increased action potential duration in IB4 -ve, neurones. The toxin did not act on tetrodotoxin-resistant (TTX-r) NaV1.8 currents; discrimination was based on tetrodotoxin-sensitive (TTX-s) Na+ channel expression. We also explored the effects of varying the holding potential on current threshold, and the effect of repetitive activation on action currents in IB4 +ve and -ve neurones. IB4 +ve neurones became more excitable with depolarization over the range -100 to -20 mV, but IB4 -ve neurones exhibited peak excitability near -55 mV, and were inexcitable at -20 mV. Eliciting action potentials at 2 Hz, we found that peak inward action current in IB4 +ve neurones was reduced, whereas changes in the current amplitude were negligible in most IB4 -ve neurones. Our findings are consistent with relatively toxin-insensitive channels including NaV1.7 being expressed in IB4 +ve neurones, whereas toxin sensitivity indicates that IB4 -ve neurones may express NaV1.1 or NaV1.2, or both. The retention of excitability at low membrane potentials, and the responses to repetitive stimulation are explained by the known preferential expression of NaV1.8 in IB4 +ve neurones, and the reduction in action current in IB4 +ve neurones with repetitive stimulation supports a novel hypothesis explaining the slowing of conduction velocity in C-fibres by the build-up of Na+ channel inactivation. Non-technical summarySmall diameter nerve fibres provide sensory input that is perceived as pain. Periods of raised impulse traffic slow the rate of impulse travel, although not all nerve fibres are affected equally, and the mechanism of slowing is still the subject of debate. We describe a novel way of pharmacologically discriminating two sub-sets of neurones that are the parent cell bodies of small diameter sensory nerves. We show that the excitability properties of these populations differ from one another and also report that repeated impulse generation can depress the excitation mechanism. These findings might explain the slowing of the rate of impulse travel in nerve fibres during periods of raised activity, and offer insights into the molecular mechanisms of pain. Sensory neurone subtypes (≤ 25 μm apparent diameter) express a variety of Na + channels, where expression is linked to action potential duration, and associated with differential IB4-lectin binding. We hypothesized that sensitivity to ATX-II might also discriminate neurones and report that 1 μ m has negligible or small effects on action potentials in IB4 +ve, but dramatically increased action potential duration in IB4 −ve, neurones. The toxin did not act on tetrodotoxin-resistant (TTX-r) Na V 1.8 currents; discrimination was based on tetrodotoxin-sensitive (TTX-s) Na + channel expression. We also explored the effects of varying the holding potential on current threshold, and the effect of repetitive activation on action currents in IB4 +ve and −ve neurones. IB4 +ve neurones became more excitable with depolarization over the range −100 to −20 mV, but IB4 −ve neurones exhibited peak excitability near −55 mV, and were inexcitable at −20 mV. Eliciting action potentials at 2 Hz, we found that peak inward action current in IB4 +ve neurones was reduced, whereas changes in the current amplitude were negligible in most IB4 −ve neurones. Our findings are consistent with relatively toxin-insensitive channels including Na V 1.7 being expressed in IB4 +ve neurones, whereas toxin sensitivity indicates that IB4 −ve neurones may express Na V 1.1 or Na V 1.2, or both. The retention of excitability at low membrane potentials, and the responses to repetitive stimulation are explained by the known preferential expression of Na V 1.8 in IB4 +ve neurones, and the reduction in action current in IB4 +ve neurones with repetitive stimulation supports a novel hypothesis explaining the slowing of conduction velocity in C-fibres by the build-up of Na + channel inactivation. Sensory neurone subtypes (≤ 25 μm apparent diameter) express a variety of Na+ channels, where expression is linked to action potential duration, and associated with differential IB4‐lectin binding. We hypothesized that sensitivity to ATX‐II might also discriminate neurones and report that 1 μm has negligible or small effects on action potentials in IB4 +ve, but dramatically increased action potential duration in IB4 −ve, neurones. The toxin did not act on tetrodotoxin‐resistant (TTX‐r) NaV1.8 currents; discrimination was based on tetrodotoxin‐sensitive (TTX‐s) Na+ channel expression. We also explored the effects of varying the holding potential on current threshold, and the effect of repetitive activation on action currents in IB4 +ve and −ve neurones. IB4 +ve neurones became more excitable with depolarization over the range −100 to −20 mV, but IB4 −ve neurones exhibited peak excitability near −55 mV, and were inexcitable at −20 mV. Eliciting action potentials at 2 Hz, we found that peak inward action current in IB4 +ve neurones was reduced, whereas changes in the current amplitude were negligible in most IB4 −ve neurones. Our findings are consistent with relatively toxin‐insensitive channels including NaV1.7 being expressed in IB4 +ve neurones, whereas toxin sensitivity indicates that IB4 −ve neurones may express NaV1.1 or NaV1.2, or both. The retention of excitability at low membrane potentials, and the responses to repetitive stimulation are explained by the known preferential expression of NaV1.8 in IB4 +ve neurones, and the reduction in action current in IB4 +ve neurones with repetitive stimulation supports a novel hypothesis explaining the slowing of conduction velocity in C‐fibres by the build‐up of Na+ channel inactivation. Non‐technical summary Small diameter nerve fibres provide sensory input that is perceived as pain. Periods of raised impulse traffic slow the rate of impulse travel, although not all nerve fibres are affected equally, and the mechanism of slowing is still the subject of debate. We describe a novel way of pharmacologically discriminating two sub‐sets of neurones that are the parent cell bodies of small diameter sensory nerves. We show that the excitability properties of these populations differ from one another and also report that repeated impulse generation can depress the excitation mechanism. These findings might explain the slowing of the rate of impulse travel in nerve fibres during periods of raised activity, and offer insights into the molecular mechanisms of pain. Sensory neurone subtypes (≤ 25 μm apparent diameter) express a variety of Na + channels, where expression is linked to action potential duration, and associated with differential IB4‐lectin binding. We hypothesized that sensitivity to ATX‐II might also discriminate neurones and report that 1 μ m has negligible or small effects on action potentials in IB4 +ve, but dramatically increased action potential duration in IB4 −ve, neurones. The toxin did not act on tetrodotoxin‐resistant (TTX‐r) Na V 1.8 currents; discrimination was based on tetrodotoxin‐sensitive (TTX‐s) Na + channel expression. We also explored the effects of varying the holding potential on current threshold, and the effect of repetitive activation on action currents in IB4 +ve and −ve neurones. IB4 +ve neurones became more excitable with depolarization over the range −100 to −20 mV, but IB4 −ve neurones exhibited peak excitability near −55 mV, and were inexcitable at −20 mV. Eliciting action potentials at 2 Hz, we found that peak inward action current in IB4 +ve neurones was reduced, whereas changes in the current amplitude were negligible in most IB4 −ve neurones. Our findings are consistent with relatively toxin‐insensitive channels including Na V 1.7 being expressed in IB4 +ve neurones, whereas toxin sensitivity indicates that IB4 −ve neurones may express Na V 1.1 or Na V 1.2, or both. The retention of excitability at low membrane potentials, and the responses to repetitive stimulation are explained by the known preferential expression of Na V 1.8 in IB4 +ve neurones, and the reduction in action current in IB4 +ve neurones with repetitive stimulation supports a novel hypothesis explaining the slowing of conduction velocity in C‐fibres by the build‐up of Na + channel inactivation. Non‐technical summary Small diameter nerve fibres provide sensory input that is perceived as pain. Periods of raised impulse traffic slow the rate of impulse travel, although not all nerve fibres are affected equally, and the mechanism of slowing is still the subject of debate. We describe a novel way of pharmacologically discriminating two sub‐sets of neurones that are the parent cell bodies of small diameter sensory nerves. We show that the excitability properties of these populations differ from one another and also report that repeated impulse generation can depress the excitation mechanism. These findings might explain the slowing of the rate of impulse travel in nerve fibres during periods of raised activity, and offer insights into the molecular mechanisms of pain. Sensory neurone subtypes (< or = 25 microm apparent diameter) express a variety of Na(+) channels, where expression is linked to action potential duration, and associated with differential IB4-lectin binding. We hypothesized that sensitivity to ATX-II might also discriminate neurones and report that 1 microm has negligible or small effects on action potentials in IB4 +ve, but dramatically increased action potential duration in IB4 ve, neurones. The toxin did not act on tetrodotoxin-resistant (TTX-r) Na(V)1.8 currents; discrimination was based on tetrodotoxin-sensitive (TTX-s) Na(+) channel expression. We also explored the effects of varying the holding potential on current threshold, and the effect of repetitive activation on action currents in IB4 +ve and ve neurones. IB4 +ve neurones became more excitable with depolarization over the range 100 to 20 mV, but IB4 ve neurones exhibited peak excitability near 55 mV, and were inexcitable at 20 mV. Eliciting action potentials at 2 Hz, we found that peak inward action current in IB4 +ve neurones was reduced, whereas changes in the current amplitude were negligible in most IB4 ve neurones. Our findings are consistent with relatively toxin-insensitive channels including Na(V)1.7 being expressed in IB4 +ve neurones, whereas toxin sensitivity indicates that IB4 ve neurones may express Na(V)1.1 or Na(V)1.2, or both. The retention of excitability at low membrane potentials, and the responses to repetitive stimulation are explained by the known preferential expression of Na(V)1.8 in IB4 +ve neurones, and the reduction in action current in IB4 +ve neurones with repetitive stimulation supports a novel hypothesis explaining the slowing of conduction velocity in C-fibres by the build-up of Na(+) channel inactivation. Sensory neurone subtypes (< or = 25 microm apparent diameter) express a variety of Na(+) channels, where expression is linked to action potential duration, and associated with differential IB4-lectin binding. We hypothesized that sensitivity to ATX-II might also discriminate neurones and report that 1 microm has negligible or small effects on action potentials in IB4 +ve, but dramatically increased action potential duration in IB4 ve, neurones. The toxin did not act on tetrodotoxin-resistant (TTX-r) Na(V)1.8 currents; discrimination was based on tetrodotoxin-sensitive (TTX-s) Na(+) channel expression. We also explored the effects of varying the holding potential on current threshold, and the effect of repetitive activation on action currents in IB4 +ve and ve neurones. IB4 +ve neurones became more excitable with depolarization over the range 100 to 20 mV, but IB4 ve neurones exhibited peak excitability near 55 mV, and were inexcitable at 20 mV. Eliciting action potentials at 2 Hz, we found that peak inward action current in IB4 +ve neurones was reduced, whereas changes in the current amplitude were negligible in most IB4 ve neurones. Our findings are consistent with relatively toxin-insensitive channels including Na(V)1.7 being expressed in IB4 +ve neurones, whereas toxin sensitivity indicates that IB4 ve neurones may express Na(V)1.1 or Na(V)1.2, or both. The retention of excitability at low membrane potentials, and the responses to repetitive stimulation are explained by the known preferential expression of Na(V)1.8 in IB4 +ve neurones, and the reduction in action current in IB4 +ve neurones with repetitive stimulation supports a novel hypothesis explaining the slowing of conduction velocity in C-fibres by the build-up of Na(+) channel inactivation.Sensory neurone subtypes (< or = 25 microm apparent diameter) express a variety of Na(+) channels, where expression is linked to action potential duration, and associated with differential IB4-lectin binding. We hypothesized that sensitivity to ATX-II might also discriminate neurones and report that 1 microm has negligible or small effects on action potentials in IB4 +ve, but dramatically increased action potential duration in IB4 ve, neurones. The toxin did not act on tetrodotoxin-resistant (TTX-r) Na(V)1.8 currents; discrimination was based on tetrodotoxin-sensitive (TTX-s) Na(+) channel expression. We also explored the effects of varying the holding potential on current threshold, and the effect of repetitive activation on action currents in IB4 +ve and ve neurones. IB4 +ve neurones became more excitable with depolarization over the range 100 to 20 mV, but IB4 ve neurones exhibited peak excitability near 55 mV, and were inexcitable at 20 mV. Eliciting action potentials at 2 Hz, we found that peak inward action current in IB4 +ve neurones was reduced, whereas changes in the current amplitude were negligible in most IB4 ve neurones. Our findings are consistent with relatively toxin-insensitive channels including Na(V)1.7 being expressed in IB4 +ve neurones, whereas toxin sensitivity indicates that IB4 ve neurones may express Na(V)1.1 or Na(V)1.2, or both. The retention of excitability at low membrane potentials, and the responses to repetitive stimulation are explained by the known preferential expression of Na(V)1.8 in IB4 +ve neurones, and the reduction in action current in IB4 +ve neurones with repetitive stimulation supports a novel hypothesis explaining the slowing of conduction velocity in C-fibres by the build-up of Na(+) channel inactivation. |
| Author | Alistair Snape James F. Pittaway Mark D. Baker |
| Author_xml | – sequence: 1 givenname: Alistair surname: Snape fullname: Snape, Alistair – sequence: 2 givenname: James F. surname: Pittaway fullname: Pittaway, James F. – sequence: 3 givenname: Mark D. surname: Baker fullname: Baker, Mark D. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19900960$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1213_ANE_0b013e3182542843 crossref_primary_10_1113_jphysiol_2010_187112 crossref_primary_10_1113_jphysiol_2011_224436 crossref_primary_10_1152_jn_00785_2011 crossref_primary_10_1016_j_bpj_2014_12_034 crossref_primary_10_1016_j_pain_2013_07_036 crossref_primary_10_1113_jphysiol_2009_185017 crossref_primary_10_1007_s00424_021_02656_6 crossref_primary_10_1152_jn_00243_2014 crossref_primary_10_1007_s00424_015_1696_2 crossref_primary_10_1007_s00424_020_02419_9 crossref_primary_10_1152_jn_00091_2012 crossref_primary_10_1161_CIRCRESAHA_112_278358 crossref_primary_10_1016_j_pain_2013_06_015 crossref_primary_10_1113_jphysiol_2011_220624 crossref_primary_10_1152_jn_00777_2012 crossref_primary_10_1111_bph_12119 crossref_primary_10_1113_jphysiol_2010_190736 crossref_primary_10_1186_1744_8069_8_69 crossref_primary_10_1016_j_jneuroim_2019_05_002 |
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| Publisher | The Physiological Society Blackwell Publishing Ltd Wiley Subscription Services, Inc Blackwell Science Inc |
| Publisher_xml | – name: The Physiological Society – name: Blackwell Publishing Ltd – name: Wiley Subscription Services, Inc – name: Blackwell Science Inc |
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| Snippet | Sensory neurone subtypes (⤠25 μm apparent diameter) express a variety of Na + channels, where expression is linked to action potential duration, and... Sensory neurone subtypes (≤ 25 μm apparent diameter) express a variety of Na+ channels, where expression is linked to action potential duration, and associated... Sensory neurone subtypes (≤ 25 μm apparent diameter) express a variety of Na + channels, where expression is linked to action potential duration, and... Sensory neurone subtypes (< or = 25 microm apparent diameter) express a variety of Na(+) channels, where expression is linked to action potential duration, and... Sensory neurone subtypes (≤ 25 µm apparent diameter) express a variety of Na+ channels, where expression is linked to action potential duration, and associated... |
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| SubjectTerms | Action Potentials - drug effects Animals Cell Size Cells, Cultured Cnidarian Venoms - toxicity Dose-Response Relationship, Drug Ganglia, Spinal - drug effects Ganglia, Spinal - physiology Neuroscience Neurotoxins - toxicity Plant Lectins - toxicity Rats Rats, Wistar Sensory Receptor Cells - cytology Sensory Receptor Cells - drug effects Sensory Receptor Cells - physiology |
| Title | Excitability parameters and sensitivity to anemone toxin ATX-II in rat small diameter primary sensory neurones discriminated by Griffonia simplicifolia isolectin IB4 |
| URI | http://jp.physoc.org/content/588/1/125.abstract https://onlinelibrary.wiley.com/doi/abs/10.1113%2Fjphysiol.2009.181107 https://www.ncbi.nlm.nih.gov/pubmed/19900960 https://www.proquest.com/docview/1545319167 https://www.proquest.com/docview/733608589 https://pubmed.ncbi.nlm.nih.gov/PMC2821554 |
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