Modification of sodium channel gating and kinetics by versutoxin from the Australian funnel-web spider Hadronyche versuta.
Identifieur interne : 002305 ( Main/Corpus ); précédent : 002304; suivant : 002306Modification of sodium channel gating and kinetics by versutoxin from the Australian funnel-web spider Hadronyche versuta.
Auteurs : G M Nicholson ; M. Willow ; M E Howden ; T. NarahashiSource :
- Pflugers Archiv : European journal of physiology [ 0031-6768 ] ; 1994.
English descriptors
- KwdEn :
- Animals (MeSH), Cations, Divalent (pharmacology), Drug Interactions (MeSH), Drug Resistance (MeSH), Electrophysiology (MeSH), Female (MeSH), Ganglia, Spinal (cytology), Ganglia, Spinal (drug effects), Homeostasis (MeSH), Ion Channel Gating (drug effects), Kinetics (MeSH), Male (MeSH), Neurons (drug effects), Neurons (metabolism), Potassium Channels (drug effects), Rats (MeSH), Rats, Sprague-Dawley (MeSH), Sodium Channels (drug effects), Sodium Channels (metabolism), Spider Venoms (pharmacology), Spiders (MeSH), Tetrodotoxin (pharmacology).
- MESH :
- chemical , drug effects : Potassium Channels, Sodium Channels.
- chemical , metabolism : Sodium Channels.
- chemical , pharmacology : Cations, Divalent, Spider Venoms, Tetrodotoxin.
- cytology : Ganglia, Spinal.
- drug effects : Ganglia, Spinal, Ion Channel Gating, Neurons.
- metabolism : Neurons.
- Animals, Drug Interactions, Drug Resistance, Electrophysiology, Female, Homeostasis, Kinetics, Male, Rats, Rats, Sprague-Dawley, Spiders.
Abstract
The effects of a neurotoxin (versutoxin VTX), purified from the venom of the Australian Blue Mountains funnel-web spider Hadronyche versuta, on the ionic currents in rat dorsal root ganglion cells were investigated under voltage-clamp conditions using the whole-cell patch-clamp technique. VTX had no effect on tetrodotoxin-resistant (TTX-R) sodium currents or potassium currents. In contrast VTX produced a dose-dependent slowing or removal of tetrodotoxin-sensitive (TTX-S) sodium current inactivation, a reduction in peak TTX-S sodium current but did not markedly slow tail current kinetics of TTX-S sodium currents. This steady-state sodium current was maintained during prolonged depolarizations at all test potentials and the reduction in sodium current amplitude produced by VTX had an apparent Ki of 37 nM. In the presence of 32 nM VTX the voltage dependence of steady-state sodium channel inactivation (h infinity) also showed a significant 7 mV shift in the voltage midpoint in the hyperpolarizing direction, with no change in the slope factor. In addition there was a steady-state or non-inactivating component present (14 +/- 2% of maximal sodium current) at prepulse potentials more depolarized than -40 mV, potentials which normally inactivate all TTX-S sodium channels. Finally, there was an observed increase in the rate of recovery from inactivation in the presence of VTX. These selective actions of VTX on sodium channel gating and kinetics are similar to those of alpha-scorpion and sea anemone toxins.
DOI: 10.1007/BF00724524
PubMed: 7816562
Links to Exploration step
pubmed:7816562Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Modification of sodium channel gating and kinetics by versutoxin from the Australian funnel-web spider Hadronyche versuta.</title><author><name sortKey="Nicholson, G M" sort="Nicholson, G M" uniqKey="Nicholson G" first="G M" last="Nicholson">G M Nicholson</name><affiliation><nlm:affiliation>Department of Biochemistry and Physiology, University of Technology, Sydney, Broadway, NSW, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Willow, M" sort="Willow, M" uniqKey="Willow M" first="M" last="Willow">M. Willow</name></author><author><name sortKey="Howden, M E" sort="Howden, M E" uniqKey="Howden M" first="M E" last="Howden">M E Howden</name></author><author><name sortKey="Narahashi, T" sort="Narahashi, T" uniqKey="Narahashi T" first="T" last="Narahashi">T. Narahashi</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1994">1994</date><idno type="RBID">pubmed:7816562</idno><idno type="pmid">7816562</idno><idno type="doi">10.1007/BF00724524</idno><idno type="wicri:Area/Main/Corpus">002305</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">002305</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Modification of sodium channel gating and kinetics by versutoxin from the Australian funnel-web spider Hadronyche versuta.</title><author><name sortKey="Nicholson, G M" sort="Nicholson, G M" uniqKey="Nicholson G" first="G M" last="Nicholson">G M Nicholson</name><affiliation><nlm:affiliation>Department of Biochemistry and Physiology, University of Technology, Sydney, Broadway, NSW, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Willow, M" sort="Willow, M" uniqKey="Willow M" first="M" last="Willow">M. Willow</name></author><author><name sortKey="Howden, M E" sort="Howden, M E" uniqKey="Howden M" first="M E" last="Howden">M E Howden</name></author><author><name sortKey="Narahashi, T" sort="Narahashi, T" uniqKey="Narahashi T" first="T" last="Narahashi">T. Narahashi</name></author></analytic><series><title level="j">Pflugers Archiv : European journal of physiology</title><idno type="ISSN">0031-6768</idno><imprint><date when="1994" type="published">1994</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cations, Divalent (pharmacology)</term><term>Drug Interactions (MeSH)</term><term>Drug Resistance (MeSH)</term><term>Electrophysiology (MeSH)</term><term>Female (MeSH)</term><term>Ganglia, Spinal (cytology)</term><term>Ganglia, Spinal (drug effects)</term><term>Homeostasis (MeSH)</term><term>Ion Channel Gating (drug effects)</term><term>Kinetics (MeSH)</term><term>Male (MeSH)</term><term>Neurons (drug effects)</term><term>Neurons (metabolism)</term><term>Potassium Channels (drug effects)</term><term>Rats (MeSH)</term><term>Rats, Sprague-Dawley (MeSH)</term><term>Sodium Channels (drug effects)</term><term>Sodium Channels (metabolism)</term><term>Spider Venoms (pharmacology)</term><term>Spiders (MeSH)</term><term>Tetrodotoxin (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Potassium Channels</term><term>Sodium Channels</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Sodium Channels</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cations, Divalent</term><term>Spider Venoms</term><term>Tetrodotoxin</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Ganglia, Spinal</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Ganglia, Spinal</term><term>Ion Channel Gating</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Drug Interactions</term><term>Drug Resistance</term><term>Electrophysiology</term><term>Female</term><term>Homeostasis</term><term>Kinetics</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Spiders</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The effects of a neurotoxin (versutoxin VTX), purified from the venom of the Australian Blue Mountains funnel-web spider Hadronyche versuta, on the ionic currents in rat dorsal root ganglion cells were investigated under voltage-clamp conditions using the whole-cell patch-clamp technique. VTX had no effect on tetrodotoxin-resistant (TTX-R) sodium currents or potassium currents. In contrast VTX produced a dose-dependent slowing or removal of tetrodotoxin-sensitive (TTX-S) sodium current inactivation, a reduction in peak TTX-S sodium current but did not markedly slow tail current kinetics of TTX-S sodium currents. This steady-state sodium current was maintained during prolonged depolarizations at all test potentials and the reduction in sodium current amplitude produced by VTX had an apparent Ki of 37 nM. In the presence of 32 nM VTX the voltage dependence of steady-state sodium channel inactivation (h infinity) also showed a significant 7 mV shift in the voltage midpoint in the hyperpolarizing direction, with no change in the slope factor. In addition there was a steady-state or non-inactivating component present (14 +/- 2% of maximal sodium current) at prepulse potentials more depolarized than -40 mV, potentials which normally inactivate all TTX-S sodium channels. Finally, there was an observed increase in the rate of recovery from inactivation in the presence of VTX. These selective actions of VTX on sodium channel gating and kinetics are similar to those of alpha-scorpion and sea anemone toxins.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">7816562</PMID><DateCompleted><Year>1995</Year><Month>02</Month><Day>08</Day></DateCompleted><DateRevised><Year>2019</Year><Month>07</Month><Day>26</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0031-6768</ISSN><JournalIssue CitedMedium="Print"><Volume>428</Volume><Issue>3-4</Issue><PubDate><Year>1994</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Pflugers Archiv : European journal of physiology</Title><ISOAbbreviation>Pflugers Arch</ISOAbbreviation></Journal><ArticleTitle>Modification of sodium channel gating and kinetics by versutoxin from the Australian funnel-web spider Hadronyche versuta.</ArticleTitle><Pagination><MedlinePgn>400-9</MedlinePgn></Pagination><Abstract><AbstractText>The effects of a neurotoxin (versutoxin VTX), purified from the venom of the Australian Blue Mountains funnel-web spider Hadronyche versuta, on the ionic currents in rat dorsal root ganglion cells were investigated under voltage-clamp conditions using the whole-cell patch-clamp technique. VTX had no effect on tetrodotoxin-resistant (TTX-R) sodium currents or potassium currents. In contrast VTX produced a dose-dependent slowing or removal of tetrodotoxin-sensitive (TTX-S) sodium current inactivation, a reduction in peak TTX-S sodium current but did not markedly slow tail current kinetics of TTX-S sodium currents. This steady-state sodium current was maintained during prolonged depolarizations at all test potentials and the reduction in sodium current amplitude produced by VTX had an apparent Ki of 37 nM. In the presence of 32 nM VTX the voltage dependence of steady-state sodium channel inactivation (h infinity) also showed a significant 7 mV shift in the voltage midpoint in the hyperpolarizing direction, with no change in the slope factor. In addition there was a steady-state or non-inactivating component present (14 +/- 2% of maximal sodium current) at prepulse potentials more depolarized than -40 mV, potentials which normally inactivate all TTX-S sodium channels. Finally, there was an observed increase in the rate of recovery from inactivation in the presence of VTX. These selective actions of VTX on sodium channel gating and kinetics are similar to those of alpha-scorpion and sea anemone toxins.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nicholson</LastName><ForeName>G M</ForeName><Initials>GM</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Physiology, University of Technology, Sydney, Broadway, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Willow</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Howden</LastName><ForeName>M E</ForeName><Initials>ME</Initials></Author><Author ValidYN="Y"><LastName>Narahashi</LastName><ForeName>T</ForeName><Initials>T</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 NS14144</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Pflugers Arch</MedlineTA><NlmUniqueID>0154720</NlmUniqueID><ISSNLinking>0031-6768</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002413">Cations, Divalent</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015221">Potassium Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015222">Sodium Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013111">Spider Venoms</NameOfSubstance></Chemical><Chemical><RegistryNumber>114264-83-4</RegistryNumber><NameOfSubstance UI="C055477">versutoxin</NameOfSubstance></Chemical><Chemical><RegistryNumber>4368-28-9</RegistryNumber><NameOfSubstance UI="D013779">Tetrodotoxin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002413" MajorTopicYN="N">Cations, Divalent</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004347" MajorTopicYN="N">Drug Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004351" MajorTopicYN="N">Drug Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004594" MajorTopicYN="N">Electrophysiology</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005727" MajorTopicYN="N">Ganglia, Spinal</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006706" MajorTopicYN="N">Homeostasis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015640" MajorTopicYN="N">Ion Channel Gating</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015221" MajorTopicYN="N">Potassium Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015222" MajorTopicYN="N">Sodium Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013111" MajorTopicYN="N">Spider Venoms</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013112" MajorTopicYN="N">Spiders</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013779" MajorTopicYN="N">Tetrodotoxin</DescriptorName><QualifierName UI="Q000494" 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