Cadmium inhibits GABA-activated ion currents by increasing intracellular calcium level in snail neurons

Research output: Contribution to journalArticle

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Abstract

Blocking of the GABA-activated chloride current by cadmium was investigated in identified nerve cells (RPeD1, RPaD1) of the pond snail (Lymnaea stagnalis L.), using a two-microelectrode voltage-clamp technique. Cd2+, at 50 μM extracellular concentration, inhibited GABA-activated chloride currents, both in normal and Ca2+-free solution. Intracellular injection of Ca2+ or the application of caffeine mimicked the inhibitory effect of Cd2+ on GABA-elicited currents. Cd2+-block was eliminated, or it was substantially decreased, when neurons were intracellularly loaded with EGTA, or when the Ca2+-release was blocked by ruthenium red. The blocking effect of Cd2+ was also eliminated by applying G-protein inhibitors: pertussis toxin, suramin or GTP-γ-S. Finally, intracellularly injected Cd2+ was ineffective at eliciting an inward current on GABA-activated currents, suggesting that the Cd2+-binding site resides extracellularly. These results suggest that cadmium inhibited GABA-activated chloride currents by increasing the intracellular Ca2+ level, by releasing it from intracellular stores and by interacting with a putative G-protein-coupled cell-surface "metal-receptor".

Original languageEnglish
Pages (from-to)205-211
Number of pages7
JournalBrain Research
Volume1008
Issue number2
DOIs
Publication statusPublished - May 22 2004

Fingerprint

Lymnaea
Cadmium
gamma-Aminobutyric Acid
Ions
Calcium
Neurons
GTP-Binding Proteins
Chlorides
Suramin
Ruthenium Red
Cadmium Chloride
Egtazic Acid
Pertussis Toxin
Cell Surface Receptors
Microelectrodes
Patch-Clamp Techniques
Guanosine Triphosphate
Caffeine
Metals
Binding Sites

Keywords

  • Cadmium
  • Excitable membranes and synaptic transmission
  • G-protein, neurone
  • GABA
  • Intracellular calcium
  • Ligand gated ion channels
  • Lymnaea stagnalis L.

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Cadmium inhibits GABA-activated ion currents by increasing intracellular calcium level in snail neurons. / Molnár, G.; Salánki, J.; Kiss, T.

In: Brain Research, Vol. 1008, No. 2, 22.05.2004, p. 205-211.

Research output: Contribution to journalArticle

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