Abstract
The ability to remember potential dangers in an environment is necessary to the survival of animals and humans. The cyclic AMP responsive element binding protein (CREB) is a key transcription factor in synaptic plasticity and memory consolidation. We have found that in CaMKIV(-/-) mice--which are deficient in a component of the calcium calmodulin-dependent protein kinase (CaMK) pathway, a major pathway of CREB activation--fear memory, but not persistent pain, was significantly reduced. CREB activation by fear conditioning and synaptic potentiation in the amygdala and cortical areas was reduced or blocked. We propose that cognitive memory related to a noxious shock can be disassociated from behavioral responses to tissue injury and inflammation.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amygdala / physiology
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Animals
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Biological Transport
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Calcium-Calmodulin-Dependent Protein Kinase Type 4
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Calcium-Calmodulin-Dependent Protein Kinases / genetics
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Calcium-Calmodulin-Dependent Protein Kinases / physiology*
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Calmodulin / metabolism
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Cell Nucleus / metabolism
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Cerebral Cortex / physiology
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Cyclic AMP Response Element-Binding Protein / physiology
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Cytoplasm / metabolism
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Electroshock
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Fear / physiology*
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Memory / physiology*
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Mice
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Mice, Inbred C57BL
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Mice, Knockout / genetics
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Neurons / metabolism
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Nociceptors / physiology
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Synapses / physiology
Substances
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Calmodulin
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Cyclic AMP Response Element-Binding Protein
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Calcium-Calmodulin-Dependent Protein Kinase Type 4
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Calcium-Calmodulin-Dependent Protein Kinases
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Camk4 protein, mouse