Source:http://linkedlifedata.com/resource/pubmed/id/16889902
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2006-9-25
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pubmed:abstractText |
Potassium channels contribute to basic neuronal excitability and modulation. Here, we examined expression patterns of the voltage-gated potassium channel Kv1.4, the nociceptive transduction channels TRPV1 and TRPV2 as well as the putative anti-nociceptive cannabinoid receptor CB1 by immunofluorescence double-labelings in sections of rat dorsal root ganglia (DRGs). Kv1.4, TRPV1 and CB1 were each detected in about one third of neurons (35.7+/-0.5%, 29.4+/-1.1% and 36.4+/-0.5%, respectively, mean diameter 19.1+/-0.3 microm). TRPV2 was present in 4.4+/-0.4% of all neurons that were significantly larger in diameter (27.4+/-0.7 microm; P < 0.001). Antibody double-labeling revealed that the majority of Kv1.4-positive neurons co-expressed TRPV1 (73.9+/-1.5%) whereas none expressed TRPV2. The largest overlap was found with CB1 (93.1+/-0.1%). CB1 expression resembled that seen for Kv1.4 since the majority of neurons expressing CB1-protein also expressed TRPV1 (69.4+/-6.5%) but not TRPV2 (0.6+/-0.3%). When CB1-mRNA was detected using in situ hybridizations an additional subset of larger neurons was labeled including 82.4+/-17.7% of the TRPV2 expressing neurons. However, co-localization of Kv1.4 with CB1-mRNA (92%, mean diameter: 18.5 microm) was essentially the same as with CB1-protein. The almost complete overlap of CB1 and Kv1.4 in nociceptive DRG neurons suggests a functional synergistic action between Kv1.4 and CB1. The potassium channel may have two important roles in nociception. As the molecular basis of A-type current it could be involved in the control of repetitive discharges at peripheral terminals and as a downstream signal transduction site of CB1 in the control of presynaptic transmitter release at central terminals.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Cannabinoid, CB1,
http://linkedlifedata.com/resource/pubmed/chemical/Shal Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/TRPV Cation Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Trpv1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Trpv2 protein, rat
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0306-4522
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
13
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pubmed:volume |
142
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
527-39
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pubmed:meshHeading |
pubmed-meshheading:16889902-Animals,
pubmed-meshheading:16889902-Blotting, Western,
pubmed-meshheading:16889902-Cell Count,
pubmed-meshheading:16889902-Cells, Cultured,
pubmed-meshheading:16889902-Ganglia, Spinal,
pubmed-meshheading:16889902-Immunohistochemistry,
pubmed-meshheading:16889902-In Situ Hybridization,
pubmed-meshheading:16889902-Neurons,
pubmed-meshheading:16889902-Rats,
pubmed-meshheading:16889902-Rats, Sprague-Dawley,
pubmed-meshheading:16889902-Receptor, Cannabinoid, CB1,
pubmed-meshheading:16889902-Shal Potassium Channels,
pubmed-meshheading:16889902-TRPV Cation Channels
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pubmed:year |
2006
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pubmed:articleTitle |
Co-expression of the voltage-gated potassium channel Kv1.4 with transient receptor potential channels (TRPV1 and TRPV2) and the cannabinoid receptor CB1 in rat dorsal root ganglion neurons.
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pubmed:affiliation |
Institute of Physiology and Pathophysiology, Johannes Gutenberg-University, Saarstrasse 21, D-55099, Mainz, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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