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  • Title: Inhibition of chloride outward transport by gadolinium in cultured rat spinal cord neurons.
    Author: Ishibashi H, Hirao K, Yamaguchi J, Nabekura J.
    Journal: Neurotoxicology; 2009 Jan; 30(1):155-9. PubMed ID: 19007810.
    Abstract:
    Gadolinium is a rare-earth lanthanide metal ion and is used as organic gadolinium complexes in magnetic resonance imaging (MRI). Although gadolinium-based MRI agents are thought to be safe in clinical use, the in vivo release of the toxic free inorganic gadolinium (Gd3+) has been reported in some patients with kidney disease. In central nervous system neurons, the inhibitory action of GABA is a consequence of relatively hyperpolarized Cl- equilibrium potential (ECl), which results from the activity of K+-Cl- co-transporter (KCC). The lanthanide ions are reported to affect GABAA receptors. However, little is known about the effect of Gd3+ on GABAA receptor function with intact intracellular Cl- concentration. In the present study, we investigated the effect of Gd3+ on GABAA receptor-mediated currents using gramicidin perforated patch recording method in cultured rat spinal cord neurons. The application of muscimol, a GABAA receptor agonist, caused outward current at a holding potential of -50 mV. Gd3+ inhibited the muscimol-induced outward current in a concentration-dependent and reversible manner. Gd3+ inhibited the maximum muscimol response but had no effect on the half-maximum concentration. The Gd3+ inhibition was accompanied by a depolarizing shift of the reversal potential. The Gd3+ action was blocked by furosemide, a blocker of both KCC and Na+-K+-Cl- co-transporter (NKCC), but not bumetanide, a specific blocker of NKCC. Gd3+ failed to inhibit the muscimol-induced outward currents recorded by conventional whole-cell patch-clamp method which cannot retain intact intracellular Cl- concentration. These results suggest that Gd3+ inhibits a KCC function and gives rise to increase in intracellular Cl- concentration. The reduction of outward chloride transport could be related to the neurotoxic effects of Gd3+.
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