Source:http://linkedlifedata.com/resource/pubmed/id/14525728
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2004-3-10
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| pubmed:abstractText |
Voltage-dependent potassium currents are important contributors to neuron excitability and thus also to hypersensitivity after tissue insult. We hypothesized that gastric ulcers would alter K(+) current properties in primary sensory neurons. The rat stomach was surgically exposed, and a retrograde tracer (1,1'-dioctadecyl-3,3,3,3'-tetramethylindocarbocyanine methanesulfonate) was injected into multiple sites in the stomach wall. Inflammation and ulcers were produced by 10 injections of 20% acetic acid (HAc) in the gastric wall. Saline (Sal) injections served as control. Nodose or T9-10 dorsal root ganglia (DRG) cells were harvested and cultured 7 days later to record whole cell K(+) currents. Gastric sensory neurons expressed transient and sustained outward currents. Gastric inflammation significantly decreased the A-type K(+) current density in DRG and nodose neurons (Sal vs. HAc-DRG: 82.9 +/- 7.9 vs. 46.5 +/- 6.1 pA/pF; nodose: 149.2 +/- 10.9 vs. 71.4 +/- 11.8 pA/pF), whereas the sustained current was not altered. In addition, there was a significant shift in the steady-state inactivation to more hyperpolarized potentials in nodose neurons (Sal vs. HAc: -76.3 +/- 1.0 vs. -83.6 +/- 2.2 mV) associated with an acceleration of inactivation kinetics. These data suggest that a reduction in K(+) currents contributes, in part, to increased neuron excitability that may lead to development of dyspeptic symptoms.
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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/4-Aminopyridine,
http://linkedlifedata.com/resource/pubmed/chemical/Elapid Venoms,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/dendrotoxin
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
0193-1857
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
286
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
G573-9
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:14525728-4-Aminopyridine,
pubmed-meshheading:14525728-Animals,
pubmed-meshheading:14525728-Cells, Cultured,
pubmed-meshheading:14525728-Elapid Venoms,
pubmed-meshheading:14525728-Electrophysiology,
pubmed-meshheading:14525728-Ganglia, Sensory,
pubmed-meshheading:14525728-Ganglia, Spinal,
pubmed-meshheading:14525728-Kinetics,
pubmed-meshheading:14525728-Male,
pubmed-meshheading:14525728-Membrane Potentials,
pubmed-meshheading:14525728-Neurons,
pubmed-meshheading:14525728-Nodose Ganglion,
pubmed-meshheading:14525728-Patch-Clamp Techniques,
pubmed-meshheading:14525728-Potassium Channel Blockers,
pubmed-meshheading:14525728-Potassium Channels,
pubmed-meshheading:14525728-Rats,
pubmed-meshheading:14525728-Rats, Sprague-Dawley,
pubmed-meshheading:14525728-Stomach Ulcer,
pubmed-meshheading:14525728-Vagus Nerve
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| pubmed:year |
2004
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| pubmed:articleTitle |
Gastric ulcers reduce A-type potassium currents in rat gastric sensory ganglion neurons.
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| pubmed:affiliation |
Department of Pharmacology, University of Iowa, Iowa City, IA 52242, USA. khoa-dang@uiowa.edu
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| pubmed:publicationType |
Journal Article,
In Vitro
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