Multiple pathways of Pb(2+) permeation in rat cerebellar granule neurones. (Articolo in rivista)

Type
Label
  • Multiple pathways of Pb(2+) permeation in rat cerebellar granule neurones. (Articolo in rivista) (literal)
Anno
  • 2001-01-01T00:00:00+01:00 (literal)
Alternative label
  • Mazzolini M. 1, Traverso S. 1, Marchetti C. 1 (2001)
    Multiple pathways of Pb(2+) permeation in rat cerebellar granule neurones.
    in Journal of neurochemistry
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Mazzolini M. 1, Traverso S. 1, Marchetti C. 1 (literal)
Pagina inizio
  • 407 (literal)
Pagina fine
  • 416 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 79 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1: CNR (literal)
Titolo
  • Multiple pathways of Pb(2+) permeation in rat cerebellar granule neurones. (literal)
Abstract
  • The pathways of lead (Pb(2+)) uptake were studied in fura-2-loaded cerebellar granule cells from 8-day-old rats. In a nominal Ca-free external bath, Pb(2+) (5-50 microM) determined an increase of the fluorescence emission ratio (R = E(340)/E(380)) even in the absence of any specific stimulus. This rise was dose-dependent, was not significantly affected by mM Mg(2+) or Ca(2+), but it was readily reversed by the membrane-permeant heavy metal chelator tetrakis(2-pyridylmethyl) ethylene-diamine (TPEN, 100 microM), indicating that it was due to Pb(2+) influx. The rate of rise, dR/dt, was increased up to a factor of 5 by depolarizing high-KCl solution, indicating a sizeable permeation through voltage-dependent channels. This effect was neither antagonized by nimodipine, nor enhanced by BayK8644, but it was slackened by omega-agatoxin IVA (200 nM), suggesting an involvement of non-L-type calcium channels. Pb(2+) influx was also stimulated by glutamic acid or NMDA in the presence of 10-30 microM glycine, but only in Mg-free solution, suggesting that glutamate channels of the NMDA type are an additional pathway of Pb(2+) uptake. Pb(2+) caused a time-, dose- and stimulus-dependent saturation of the dye, whose intracellular concentration is approximately 10 microM, indicating that intracellular Pb(2+) can readily reach a concentration in the micromolar range. These results indicate that the particular vulnerability of neurones to Pb(2+) poisoning is linked to the presence of specific transport systems, which mediate the rapid uptake of Pb(2+) into the neurone. (literal)
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