Linked Life Data

11489454

Source:http://linkedlifedata.com/resource/pubmed/id/11489454

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-8-7
pubmed:abstractText
5-hydroxytryptamine (5-HT) has been reported to modulate analgesia produced by opioids or electrical stimulation of the periaqueductal gray (PAG). 5-HT increases K+ conductance and inhibits the firing activity of the PAG neurons. We examined the electrophysiological and pharmacological characteristics of the K+ current involved in 5-HT-induced hyperpolarization of dissociated rat PAG neurons. Among the neurons tested, 5-HT activated inward K+ currents in 30-40%, whilst the remaining 60-70% did not respond to 5-HT. 5-HT activated an inwardly rectifying K+ current (I5-HT) in a concentration- and voltage-dependent manner. I5-HT was mimicked by a 5-HT1A receptor selective agonist, 8-OH-DPAT, and was reversibly blocked by a 5-HT1A receptor antagonist, piperazine maleate, but not by a 5-HT2 receptor antagonist, ketanserin. I5-HT was sensitive to K+ channel blockers such as quinine and Ba2+, but insensitive to 4-aminopyridine, Cs+ and tetraethylammonium. I5-HT was inhibited by GDP(beta)s and was irreversibly activated by GTP(gamma)s. I5-HT was significantly suppressed by N-ethylmaleimide and pertussis toxin, but not by cholera toxin. Second messenger modulators such as staurosporin, forskolin, and phorbol-12-myristate-13-acetate did not alter I5-HT. The present study indicates that 5-HT-induced hyperpolarization of the PAG neurons results from activation of the pertussis toxin-sensitive G-protein-coupled inwardly rectifying K+ currents through 5-HT1A receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0028-3908
pubmed:author
pubmed:issnType
Print
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
175-85
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:11489454-Animals, pubmed-meshheading:11489454-Female, pubmed-meshheading:11489454-Free Radical Scavengers, pubmed-meshheading:11489454-G Protein-Coupled Inwardly-Rectifying Potassium Channels, pubmed-meshheading:11489454-GTP-Binding Proteins, pubmed-meshheading:11489454-Male, pubmed-meshheading:11489454-Neurons, pubmed-meshheading:11489454-Periaqueductal Gray, pubmed-meshheading:11489454-Potassium Channels, pubmed-meshheading:11489454-Potassium Channels, Inwardly Rectifying, pubmed-meshheading:11489454-Rats, pubmed-meshheading:11489454-Rats, Sprague-Dawley, pubmed-meshheading:11489454-Receptors, Serotonin, pubmed-meshheading:11489454-Receptors, Serotonin, 5-HT1, pubmed-meshheading:11489454-Serotonin, pubmed-meshheading:11489454-Serotonin Antagonists, pubmed-meshheading:11489454-Serotonin Receptor Agonists
pubmed:year
2001
pubmed:articleTitle
5-HT1A receptor-mediated activation of G-protein-gated inwardly rectifying K+ current in rat periaqueductal gray neurons.
pubmed:affiliation
Department of Physiology, College of Medicine, Kyung Hee University, Seoul 130-701, South Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't