Mercury (Hg2+) decreases voltage-gated calcium channel currents in rat DRG and Aplysia neurons

M. Pekel, B. Platt, Dietrich Busselberg

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Inorganic mercury (Hg2+) reduced voltage-gated calcium channel currents irreversibility in two different preparations. In cultured rat dorsal root ganglion (DRG) neurons, studied with the whole cell patch clamp technique, a rapid concentration-dependent decrease in the L/N-type currents to a steady state was observed with an IC50 of 1.1 μM and a Hill coefficient of 1.3 T-currents were blocked with Hg2+ in the same concentration range (0.5-2 μM). With increasing Hg2+ concentrations a slow membrane current was additionally activated most obviously at concentrations over 2 μM Hg2+. This current was irreversible and might be due to the opening of other (non-specific) ion channels by Hg2+. The current-voltage (I-V) relation of DRG neurons shifted to more positive values, suggesting a binding of Hg2+ to the channel protein and/or modifying its gating properties. In neurons of the abdominal ganglion of Aplysia californica, studied with the two electrode voltage clamp technique, a continous decrease of calcium channel currents was seen even with the lowest used concentration of Hg2+ (5 μM). A steady state was not reached and the effect was irreversible without any change on resting membrane currents, even with high concentrations (up to 50 μM). No shift of the I-V relation of the calcium channel currents was observed. Effects on voltage-activated calcium channel currents with Hg2+ concentrations such low have not been reported before. We conclude that neurotoxic effects of inorganic mercury could be partially due to the irreversible blockade of voltage-activated calcium channels.

Original languageEnglish
Pages (from-to)121-126
Number of pages6
JournalBrain Research
Issue number1-2
Publication statusPublished - 31 Dec 1993
Externally publishedYes



  • Aplysia neuron
  • Calcium channel current
  • Mercury
  • Rat dorsal root ganglion (DRG) neuron

ASJC Scopus subject areas

  • Neuroscience(all)

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