Abstract
Regulated expression of a constitutively active form of cAMP response element-binding protein (CREB), VP16-CREB, lowers the threshold for the late phase of long-term potentiation in the Schaffer collateral pathway in a de novo gene expression-independent manner, and increases the excitability and reduces afterhyperpolarization of neurons at the amygdala and the hippocampus. We explore the consequences of these changes on the consolidation of fear conditioning and find that the expression of VP16-CREB can bypass the requirement for de novo gene expression associated with long-term memory formation, suggesting that CREB-dependent gene expression is sufficient for fear memory consolidation.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Amygdala / cytology*
-
Analysis of Variance
-
Animals
-
Anisomycin / pharmacology
-
Biophysical Phenomena
-
Calcium-Calmodulin-Dependent Protein Kinase Type 2 / genetics
-
Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism
-
Conditioning, Classical / physiology
-
Cues*
-
Cyclic AMP Response Element-Binding Protein / genetics
-
Cyclic AMP Response Element-Binding Protein / metabolism*
-
Electric Stimulation
-
Fear*
-
Gene Expression Regulation / drug effects
-
Gene Expression Regulation / genetics*
-
Gene Expression Regulation / physiology
-
Herpes Simplex Virus Protein Vmw65 / genetics
-
Hippocampus / cytology
-
In Vitro Techniques
-
Long-Term Potentiation / drug effects
-
Long-Term Potentiation / genetics
-
Memory / physiology*
-
Mice
-
Mice, Transgenic
-
Neurons / drug effects
-
Neurons / physiology*
-
Patch-Clamp Techniques / methods
-
Protein Synthesis Inhibitors / pharmacology
Substances
-
Cyclic AMP Response Element-Binding Protein
-
Herpes Simplex Virus Protein Vmw65
-
Protein Synthesis Inhibitors
-
Anisomycin
-
Calcium-Calmodulin-Dependent Protein Kinase Type 2