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Cu2+‐ions are known to interfere with γ‐aminobutyric acid (GABA)‐ and glutamate‐operated ion channels from experiments with isolated neurons. Such actions are likely involved in the pathophysiology of Wilson's disease. We have now studied the effects of Cu2+ in the CA 1 region of hippocampal slices. Field excitatory postsynaptic potential (EPSP) slopes in the CA1 region were unaffected by 1 μM Cu2+ but were depressed by 10 μM (to 85%) and 100 μM (to 50%). A paired‐pulse test revealed no difference in facilitation in the presence or absence of Cu2+, indicating a postsynaptic action. A late component of intracellularly registered EPSPs in Mg2+‐free solution was also reduced by Cu2+. The N‐methyl‐D‐aspartate (NMDA) component of the field EPSP, isolated by adding CNQX and bicuculline in Mg2+‐free solution, was reduced to 69% of control by 1 μM and to 50% of control by 10 μM Cu2+. Long‐term potentiation, evoked by 3 × 50 pulses at 100 Hz, 20 s interval amounted to 132 ± 11% 90 min after tetanization under control conditions but was absent in the presence of 1 μM Cu2+ in the bath. Thus low concentrations of copper can selectively reduce NMDA‐mediated potentials and synaptic plasticity. Hippocampus 1997;7:666–669. © 1997 Wiley‐Liss, Inc.
Hippocampus – Wiley
Published: Jan 1, 1997
Keywords: ; ;
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