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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
24
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pubmed:dateCreated |
1999-2-25
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pubmed:abstractText |
A tetrodotoxin-resistant voltage-gated Na+ current (TTX-R INa) appears to be the current primarily responsible for action potential generation in the cell body and terminals of nociceptive afferents. Although other voltage-gated Na+ currents are modulated by the activation of protein kinase C (PKC), protein kinase A (PKA), or both, the second messenger pathways involved in the modulation of TTX-R INa are still being defined. We have examined the modulation of TTX-R INa in isolated sensory neurons with whole-cell voltage-clamp recording. Activation of either PKC or PKA increased TTX-R INa. PKA activation also produced a leftward shift in the conductance-voltage relationship of TTX-R INa and an increase in the rates of current activation, deactivation, and inactivation. Inhibitors of PKC decreased TTX-R INa, whereas inhibitors of PKA had no effect on the current. Investigating the interaction between PKC and PKA revealed that although inhibitors of PKA had little effect on PKC-induced modulation of TTX-R INa, inhibitors of PKC significantly attenuated PKA-induced modulation of the current. Finally, although PGE2-induced modulation of TTX-R INa was more similar to PKA-induced modulation of the current than to PKC-induced modulation, PGE2-induced effects were inhibited by inhibitors of both PKC and PKA. Thus, although TTX-R INa is a common target for cellular processes involving the activation of either PKA or PKC, PKC activity is necessary to enable subsequent PKA-mediated modulation of TTX-R INa.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP-Dependent Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0270-6474
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
18
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
10345-55
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:9852572-Animals,
pubmed-meshheading:9852572-Cells, Cultured,
pubmed-meshheading:9852572-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:9852572-Dinoprostone,
pubmed-meshheading:9852572-Enzyme Activation,
pubmed-meshheading:9852572-Ganglia, Spinal,
pubmed-meshheading:9852572-Male,
pubmed-meshheading:9852572-Neurons, Afferent,
pubmed-meshheading:9852572-Protein Kinase C,
pubmed-meshheading:9852572-Rats,
pubmed-meshheading:9852572-Rats, Sprague-Dawley,
pubmed-meshheading:9852572-Sodium,
pubmed-meshheading:9852572-Sodium Channels,
pubmed-meshheading:9852572-Tetrodotoxin
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pubmed:year |
1998
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pubmed:articleTitle |
Modulation of TTX-R INa by PKC and PKA and their role in PGE2-induced sensitization of rat sensory neurons in vitro.
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pubmed:affiliation |
Department of Oral and Craniofacial Biological Sciences, University of Maryland, Baltimore Dental School, Baltimore, Maryland 21201, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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