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The Journal of Neuroscience, January 1, 2001, 21(1):356-362
Retrograde Amnesia for Spatial Memory Induced by NMDA
Receptor-Mediated Long-Term Potentiation
Vegard Heimly
Brun1,
Kristin
Ytterbø1,
Richard
G. M.
Morris2,
May-Britt
Moser1, and
Edvard I.
Moser1
1 Department of Psychology, Norwegian University of
Science and Technology, 7491 Trondheim, Norway, and
2 Department of Neuroscience, University of Edinburgh,
Edinburgh EH8 9LE, Scotland, United Kingdom
If information is stored as distributed patterns of synaptic
weights in the hippocampal formation, retention should be vulnerable to
electrically induced long-term potentiation (LTP) of hippocampal synapses after learning. This prediction was tested by training animals
in a spatial water maze task and then delivering bursts of
high-frequency (HF) or control stimulation to the perforant path in the
angular bundle. High-frequency stimulation induced LTP in the dentate
gyrus and probably also at other hippocampal termination sites.
Retention in a later probe test was disrupted. When the competitive
NMDA receptor antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) was administered before the high-frequency stimulation, water maze retention was unimpaired. CPP administration blocked the
induction of LTP. Thus, high-frequency stimulation of hippocampal afferents disrupts memory retention only when it induces a change in
the spatial pattern of synaptic weights. The NMDA receptor dependency
of this retrograde amnesia is consistent with the synaptic plasticity
and memory hypothesis.
Key words:
memory; spatial memory; synaptic plasticity; hippocampus; dentate gyrus; LTP; NMDA receptor; CPP; water maze; rat; saturation; retrograde amnesia
Copyright © 2001 Society for Neuroscience 0270-6474/01/211356-07$05.00/0
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