Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-10-16
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
291
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
399-406
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Potentiation and inhibition of subtypes of neuronal nicotinic acetylcholine receptors by Pb2+.
pubmed:affiliation
Research Institute of Toxicology, Utrecht University, Netherlands.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't