Journal
CEREBRAL CORTEX
Volume 23, Issue 4, Pages 932-939Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/cercor/bhs086
Keywords
experience; learning; long-term potentiation; synaptic plasticity
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Funding
- Science Foundation Ireland [10/IN.1/B3001]
- Health Research Board of Ireland [COEN/2011/11]
- European Commission [MEMOLOAD 201159]
- Science Foundation Ireland (SFI) [10/IN.1/B3001] Funding Source: Science Foundation Ireland (SFI)
- Health Research Board (HRB) [COEN-2011-11] Funding Source: Health Research Board (HRB)
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Both electrically induced synaptic long-term potentiation (LTP) and long-term depression have been extensively studied as models of the cellular basis of learning and memory mechanisms. Recently, considerable interest has been generated by the possibility that the activity-dependent persistent reversal of previously established synaptic LTP (depotentiation) may play a role in the time- and state-dependent erasure of memory. Here, we examined the requirement for glutamate receptor activation in experience-induced reversal of previously established LTP in the CA1 area of the hippocampus of freely behaving rats. Continuous exploration of non-aversive novelty for similar to 30 min, which was associated with hippocampal activation as measured by increased theta power in the electroencephalogram, triggered a rapid and persistent reversal of high frequency stimulation-induced LTP both at apical and basal synapses. Blockade of metabotropic glutamate (mGlu) receptors with mGlu5 subtype-selective antagonists, or N-methyl-D-aspartate (NMDA) receptors with GluN2B subunit-selective antagonists, prevented novelty-induced depotentiation. These findings strongly indicate that activation of both mGlu5 receptors and GluN2B-containing NMDA receptors is required for experience-triggered induction of depotentiation at CA3-CA1 synapses. The mechanistic concordance of the present and previous studies of experience-induced and electrically induced synaptic depotentiation helps to integrate our understanding of the neurophysiological underpinnings of learning and memory.
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