Mercury (Hg2+) and zinc (Zn2+)

Two divalent cations with different actions on voltage-activated calcium channel currents

Dietrich Busselberg, M. Pekel, D. Michael, B. Platt

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

1. We examined the actions of mercury (Hg2+) and zinc (Zn2+) on voltage-activated calcium channel currents of cultured rat dorsal root ganglion (DRG) neurons, using the whole-cell patch clamp technique. 2. Micromolar concentrations of both cations reduced voltage-activated calcium channel currents. Calcium channel currents elicited by voltage jumps from a holding potential of -80 to 0 mV (mainly L- and N-currents) were reduced by Hg2+ and Zn2+. The threshold concentration for Hg2+ effects was 0.1 μM and that for Zn2+ was 10 μM. Voltage-activated calcium channel currents were abolished (>80%) with 5 μM Hg2+ or 200 μM Zn2+. The peak calcium current was reduced to 50% (IC50) by 1.1 μM Hg2+ or 69 μM Zn2+. While Zn2+ was much more effective in reducing the T-type calcium channel current-activated by jumping from -80 to -35 mV-Hg2+ showed some increased effectiveness in reducing this current. 3. The effects of both cations occurred rapidly and a steady state was reached within 1-3 min. While the action of Zn2+ was not dependent on an open channel state, Hg2+ effects depended partially on channel activation. 4. While both metal cations reduced the calcium channel currents over the whole voltage range, some charge screening effects were detected with Hg2+ and with higher concentrations (>100 μM) of Zn2+. 5. As Zn2+ in the concentration range used had no influence on resting membrane currents, Hg2+ caused a clear inward current at concentrations ≥μM. 6. In the present study we discuss whether the actions of both metals on voltage-activated calcium channel currents are mediated through the same binding site and how they may be related to their neurotoxic effects.

Original languageEnglish
Pages (from-to)675-687
Number of pages13
JournalCellular and Molecular Neurobiology
Volume14
Issue number6
DOIs
Publication statusPublished - Dec 1994
Externally publishedYes

Fingerprint

Divalent Cations
Calcium Channels
Mercury
Zinc
Electric potential
Cations
Metals
T-Type Calcium Channels
Clamping devices
Spinal Ganglia
Patch-Clamp Techniques
Inhibitory Concentration 50
Neurons
Rats
Screening
Chemical activation
Binding Sites
Calcium
Membranes

Keywords

  • mercury (Hg)
  • metal neurotoxicity
  • voltage-activated calcium channel currents
  • zinc (Zn)

ASJC Scopus subject areas

  • Neuroscience(all)
  • Genetics
  • Clinical Biochemistry
  • Cell Biology

Cite this

Mercury (Hg2+) and zinc (Zn2+) : Two divalent cations with different actions on voltage-activated calcium channel currents. / Busselberg, Dietrich; Pekel, M.; Michael, D.; Platt, B.

In: Cellular and Molecular Neurobiology, Vol. 14, No. 6, 12.1994, p. 675-687.

Research output: Contribution to journalArticle

@article{0474973243954f49a53d773393252695,
title = "Mercury (Hg2+) and zinc (Zn2+): Two divalent cations with different actions on voltage-activated calcium channel currents",
abstract = "1. We examined the actions of mercury (Hg2+) and zinc (Zn2+) on voltage-activated calcium channel currents of cultured rat dorsal root ganglion (DRG) neurons, using the whole-cell patch clamp technique. 2. Micromolar concentrations of both cations reduced voltage-activated calcium channel currents. Calcium channel currents elicited by voltage jumps from a holding potential of -80 to 0 mV (mainly L- and N-currents) were reduced by Hg2+ and Zn2+. The threshold concentration for Hg2+ effects was 0.1 μM and that for Zn2+ was 10 μM. Voltage-activated calcium channel currents were abolished (>80{\%}) with 5 μM Hg2+ or 200 μM Zn2+. The peak calcium current was reduced to 50{\%} (IC50) by 1.1 μM Hg2+ or 69 μM Zn2+. While Zn2+ was much more effective in reducing the T-type calcium channel current-activated by jumping from -80 to -35 mV-Hg2+ showed some increased effectiveness in reducing this current. 3. The effects of both cations occurred rapidly and a steady state was reached within 1-3 min. While the action of Zn2+ was not dependent on an open channel state, Hg2+ effects depended partially on channel activation. 4. While both metal cations reduced the calcium channel currents over the whole voltage range, some charge screening effects were detected with Hg2+ and with higher concentrations (>100 μM) of Zn2+. 5. As Zn2+ in the concentration range used had no influence on resting membrane currents, Hg2+ caused a clear inward current at concentrations ≥μM. 6. In the present study we discuss whether the actions of both metals on voltage-activated calcium channel currents are mediated through the same binding site and how they may be related to their neurotoxic effects.",
keywords = "mercury (Hg), metal neurotoxicity, voltage-activated calcium channel currents, zinc (Zn)",
author = "Dietrich Busselberg and M. Pekel and D. Michael and B. Platt",
year = "1994",
month = "12",
doi = "10.1007/BF02088676",
language = "English",
volume = "14",
pages = "675--687",
journal = "Cellular and Molecular Neurobiology",
issn = "0272-4340",
publisher = "Springer New York",
number = "6",

}

TY - JOUR

T1 - Mercury (Hg2+) and zinc (Zn2+)

T2 - Two divalent cations with different actions on voltage-activated calcium channel currents

AU - Busselberg, Dietrich

AU - Pekel, M.

AU - Michael, D.

AU - Platt, B.

PY - 1994/12

Y1 - 1994/12

N2 - 1. We examined the actions of mercury (Hg2+) and zinc (Zn2+) on voltage-activated calcium channel currents of cultured rat dorsal root ganglion (DRG) neurons, using the whole-cell patch clamp technique. 2. Micromolar concentrations of both cations reduced voltage-activated calcium channel currents. Calcium channel currents elicited by voltage jumps from a holding potential of -80 to 0 mV (mainly L- and N-currents) were reduced by Hg2+ and Zn2+. The threshold concentration for Hg2+ effects was 0.1 μM and that for Zn2+ was 10 μM. Voltage-activated calcium channel currents were abolished (>80%) with 5 μM Hg2+ or 200 μM Zn2+. The peak calcium current was reduced to 50% (IC50) by 1.1 μM Hg2+ or 69 μM Zn2+. While Zn2+ was much more effective in reducing the T-type calcium channel current-activated by jumping from -80 to -35 mV-Hg2+ showed some increased effectiveness in reducing this current. 3. The effects of both cations occurred rapidly and a steady state was reached within 1-3 min. While the action of Zn2+ was not dependent on an open channel state, Hg2+ effects depended partially on channel activation. 4. While both metal cations reduced the calcium channel currents over the whole voltage range, some charge screening effects were detected with Hg2+ and with higher concentrations (>100 μM) of Zn2+. 5. As Zn2+ in the concentration range used had no influence on resting membrane currents, Hg2+ caused a clear inward current at concentrations ≥μM. 6. In the present study we discuss whether the actions of both metals on voltage-activated calcium channel currents are mediated through the same binding site and how they may be related to their neurotoxic effects.

AB - 1. We examined the actions of mercury (Hg2+) and zinc (Zn2+) on voltage-activated calcium channel currents of cultured rat dorsal root ganglion (DRG) neurons, using the whole-cell patch clamp technique. 2. Micromolar concentrations of both cations reduced voltage-activated calcium channel currents. Calcium channel currents elicited by voltage jumps from a holding potential of -80 to 0 mV (mainly L- and N-currents) were reduced by Hg2+ and Zn2+. The threshold concentration for Hg2+ effects was 0.1 μM and that for Zn2+ was 10 μM. Voltage-activated calcium channel currents were abolished (>80%) with 5 μM Hg2+ or 200 μM Zn2+. The peak calcium current was reduced to 50% (IC50) by 1.1 μM Hg2+ or 69 μM Zn2+. While Zn2+ was much more effective in reducing the T-type calcium channel current-activated by jumping from -80 to -35 mV-Hg2+ showed some increased effectiveness in reducing this current. 3. The effects of both cations occurred rapidly and a steady state was reached within 1-3 min. While the action of Zn2+ was not dependent on an open channel state, Hg2+ effects depended partially on channel activation. 4. While both metal cations reduced the calcium channel currents over the whole voltage range, some charge screening effects were detected with Hg2+ and with higher concentrations (>100 μM) of Zn2+. 5. As Zn2+ in the concentration range used had no influence on resting membrane currents, Hg2+ caused a clear inward current at concentrations ≥μM. 6. In the present study we discuss whether the actions of both metals on voltage-activated calcium channel currents are mediated through the same binding site and how they may be related to their neurotoxic effects.

KW - mercury (Hg)

KW - metal neurotoxicity

KW - voltage-activated calcium channel currents

KW - zinc (Zn)

UR - http://www.scopus.com/inward/record.url?scp=0028671803&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028671803&partnerID=8YFLogxK

U2 - 10.1007/BF02088676

DO - 10.1007/BF02088676

M3 - Article

VL - 14

SP - 675

EP - 687

JO - Cellular and Molecular Neurobiology

JF - Cellular and Molecular Neurobiology

SN - 0272-4340

IS - 6

ER -