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Suppression of long‐term potentiation in hippocampal slices by copper

Suppression of long‐term potentiation in hippocampal slices by copper 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hippocampus Wiley

Suppression of long‐term potentiation in hippocampal slices by copper

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References (17)

Publisher
Wiley
Copyright
Copyright © 1997 Wiley Subscription Services
ISSN
1050-9631
eISSN
1098-1063
DOI
10.1002/(SICI)1098-1063(1997)7:6<666::AID-HIPO8>3.0.CO;2-C
Publisher site
See Article on Publisher Site

Abstract

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.

Journal

HippocampusWiley

Published: Jan 1, 1997

Keywords: ; ;

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