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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1992-7-20
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pubmed:abstractText |
The mechanism underlying the slowed activation of the high voltage-activated Ca2+ current (HVA-ICa) in the presence of (-)-baclofen was studied in cultured neurons of rat dorsal root ganglia. The decay phase of the baclofen-sensitive component of HVA-ICa was described by a sum of two exponential functions. Although the inhibited portion in the amplitude of the baclofen-sensitive component of HVA-ICa was increased in a concentration-dependent manner, the two decay time constants remained unaffected regardless of the concentration of baclofen. Furthermore, the baclofen-sensitive component of HVA-ICa was largely inactivated by a depolarizing prepulse (-30 mV for 0.5 s). These results support the notion that the slowed activation of the HVA-ICa in the presence of baclofen is due to a preferential inhibition of the inactivating component of HVA-ICa rather than due to voltage-dependent unblocking of a single population of HVA-ICa.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0304-3940
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
139
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
261-4
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1319018-Animals,
pubmed-meshheading:1319018-Baclofen,
pubmed-meshheading:1319018-Calcium Channels,
pubmed-meshheading:1319018-Cells, Cultured,
pubmed-meshheading:1319018-Electrophysiology,
pubmed-meshheading:1319018-Ganglia, Spinal,
pubmed-meshheading:1319018-Neurons, Afferent,
pubmed-meshheading:1319018-Rats,
pubmed-meshheading:1319018-Receptors, GABA-A,
pubmed-meshheading:1319018-gamma-Aminobutyric Acid
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pubmed:year |
1992
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pubmed:articleTitle |
The mechanism of GABAB-mediated slowing of the activation phase of high voltage-activated Ca2+ channels in rat sensory neurons.
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pubmed:affiliation |
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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