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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1996-10-16
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pubmed:abstractText |
Effects of inorganic lead (Pb2+) on defined subtypes of neuronal nicotinic acetylcholine receptors have been investigated. Voltage clamp experiments have been performed on Xenopus oocytes expressing alpha 3 beta 2, alpha 3 beta 4 and alpha 4 beta 2 neuronal nicotinic acetylcholine receptor subunit combinations. In oocytes expressing the alpha 3 beta 2 subunit combination Pb2+ enhances the peak amplitude of nicotinic acetylcholine receptor-mediated inward currents evoked by superfusion with 100 microM acetylcholine. At concentrations of 1-250 microM, Pb2+ potentiates alpha 3 beta 2 receptor-mediated inward current concentration dependently by a factor of 1.1-11.0. Inward currents evoked by low (3 microM) and high (1 mM) concentrations of acetylcholine are potentiated to a similar extent. Conversely, in oocytes expressing the alpha 3 beta 4 subunit combination Pb2+ inhibits the nicotinic receptor-mediated inward currents evoked with 100 microM acetylcholine. Inhibitory effects are observed in the concentration range of 1 nM-100 microM Pb2+ but the degree of inhibition varies between oocytes. A similar inhibition of the alpha 4 beta 2 nicotinic receptor-mediated inward current by Pb2+ indicates that alpha as well as beta subunits are involved in the potentiating and inhibitory effects. Possible reasons for the variation in the inhibitory effects of Pb2+ on alpha 3 beta 4 and alpha 4 beta 2 nicotinic receptor-mediated inward currents have been investigated and are discussed. The divalent cations Ca2+ and Mg2+ potentiate both alpha 3 beta 2 and alpha 3 beta 4 nicotinic receptor-mediated inward currents. The distinct modulation of receptor function by Pb2+ and by Ca2+ and Mg2+ and the dependence of the modulatory effect of Pb2+ on subunit composition suggest that Pb2+ interacts with multiple sites on the alpha and beta subunits of neuronal nicotinic acetylcholine receptors.
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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/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Lead,
http://linkedlifedata.com/resource/pubmed/chemical/Magnesium,
http://linkedlifedata.com/resource/pubmed/chemical/Nicotinic Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nicotinic
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0014-2999
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
30
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pubmed:volume |
291
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
399-406
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8719426-Animals,
pubmed-meshheading:8719426-Calcium,
pubmed-meshheading:8719426-Electrophysiology,
pubmed-meshheading:8719426-Ion Channels,
pubmed-meshheading:8719426-Lead,
pubmed-meshheading:8719426-Magnesium,
pubmed-meshheading:8719426-Neurons,
pubmed-meshheading:8719426-Nicotinic Antagonists,
pubmed-meshheading:8719426-Receptors, Nicotinic,
pubmed-meshheading:8719426-Synaptic Transmission,
pubmed-meshheading:8719426-Transfection,
pubmed-meshheading:8719426-Xenopus laevis
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pubmed:year |
1995
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pubmed:articleTitle |
Potentiation and inhibition of subtypes of neuronal nicotinic acetylcholine receptors by Pb2+.
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pubmed:affiliation |
Research Institute of Toxicology, Utrecht University, Netherlands.
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pubmed:publicationType |
Journal Article,
Comparative Study,
In Vitro,
Research Support, Non-U.S. Gov't
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