Journal
NEURON
Volume 51, Issue 6, Pages 823-834Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2006.08.026
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Funding
- NIDCD NIH HHS [R01 DC004154, R01 DC04154, F31 DC07006] Funding Source: Medline
- NINDS NIH HHS [P01 NS053862] Funding Source: Medline
- PHS HHS [R01] Funding Source: Medline
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The number and diversity of plasticity mechanisms in the brain raises a central question: does a neural circuit store all memories by stereotyped application of the available plasticity mechanisms, or can subsets of these mechanisms be selectively engaged for specific memories? The uniform architecture of the cerebellum has inspired the idea that plasticity mechanisms like cerebellar long-term depression (LTD) contribute universally to memory storage. To test this idea, we investigated a set of closely related, cerebellum-dependent motor memories. In mutant mice lacking Ca2+/calmodulin-dependent protein kinase IV (CaMKIV), the maintenance of cerebellar LTD is abolished. Although memory for an increase in the gain of the vestibulo-ocular reflex (VOR) induced with high-frequency stimuli was impaired in these mice, memories for decreases in VOR gain and increases in gain induced with low-frequency stimuli were intact. Thus, a particular plasticity mechanism need not support all cerebellum-dependent memories, but can be engaged selectively according to the parameters of training.
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