Journal
LEARNING & MEMORY
Volume 14, Issue 1-2, Pages 75-83Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/lm.356607
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Funding
- MRC [G0400983] Funding Source: UKRI
- Medical Research Council [G0400983] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
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alpha CaMKIIT286A mutant mice lack long-term potentiation (LTP) in the hippocampal CA1 region and are impaired in spatial learning. In situ hybridization confirms that the mutant mice show the same developmental expression of alpha CaMKII as their wild-type littermates. A simple hypothesis would suggest that if LTP is a substrate for learning, then enriching the environment should cause learning-dependent changes in wild-type mice that have LTP. Such changes would not be seen in LTP-deficient alpha CaMKIIT286A mutants. Excitatory synaptic currents in CA1 neurons, recorded with patch clamp in brain slices, revealed that enrichment induces an increase in glutamate release probability and a decreased miniature current amplitude. Confocal microscopy also showed dendritic spine density to be reduced. However, contrary to the hypothesis above, these enrichment-induced changes occur only in the mutant mice and are not detectable in wild-type littermates. We suggest that enrichment induces alpha CaMKII-independent changes in both wild-type and mutant mice. Such changes may be subsequently reversed in wild-type animals via alpha CaMKII-dependent mechanisms, such as LTP. Reversal of plasticity has long been hypothesized to be essential for the hippocampus to maintain its role in memory processing. The inability to reverse plasticity in alpha CaMKIIT286A mutant mice would then result in impairment of spatial learning.
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