CREB and the formation of long-term memory

  title={CREB and the formation of long-term memory},
  author={Jerry C. P. Yin and Tim Tully},
  journal={Current Opinion in Neurobiology},

CREB Responsive Transcription and Memory Formation

This chapter will review the molecular biology of CREB genes, before summarizing the work that demonstrates CREB is an important factor in memory formation, and addressing the more complex issue of why this requirement remains controversial.

Serine 133 phosphorylation is not required for hippocampal CREB-mediated transcription and behavior.

It is shown that CREB phosphorylation at Ser133 is not necessary for CREB binding to CRE sites, CREB-mediated transcription, or CREb-mediated behavioral phenotypes associated with learning and memory.

dCREB2-Mediated Enhancement of Memory Formation

It is reaffirmed that overexpression of a dCREB2 activator can enhance memory formation and the complexity of this behavioral enhancement is illustrated.

MAPK regulation of gene expression in the central nervous system.

These studies indicate a critical role for the MAPK cascade in the regulation of CREB phosphorylation in the hippocampus, and evaluate the capacity of theMAPK ERK (extracellular signal-regulated kinase) to regulate phosphorylated cAMP response element binding protein in hippocampal area CA1.

CREB-mediated Enhancement of Hippocampus-dependent Memory Consolidation and Reconsolidation

A gain-of-function approach is used to show that CREB (and CREB-coactivator CRTC1) can facilitate both synaptic and systems consolidation and reconsolidation in mice with brain-wide disrupted CREB function.

Viral‐mediated expression of a constitutively active form of CREB in hippocampal neurons increases memory

There is direct evidence that a brief increase in CREB‐dependent transcription in either CA1 or DG neurons, using in vivo viral vectors, is sufficient to boost memory for contextual representations, as tested in the contextual fear conditioning task, without affecting motor, pain, or anxiety behaviors.

The Role of cAMP Response Element-Binding Protein in Drosophila Long-Term Memory

It is shown that the dCREB2-a transgene originally reported to enhance LTM carries a mutation that produces a translational reading-frame shift with the consequent formation of a stop codon at predicted amino acid position 79, and an alternative model for the role of d CREB in Drosophila LTM is proposed.

Nuclear Calcium/Calmodulin Regulates Memory Consolidation

It is shown that nuclear Ca2+/CaM signaling plays a critical role in memory consolidation in the mouse and is associated with diminished neuronal activity-induced phosphorylation of cAMP response element-binding protein.



Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons.

Activation of PKA may be a component of the mechanism that generates L-LTP, and analogs of cAMP induced a potentiation that blocked naturally induced L- LTP, which was blocked by inhibitors of protein synthesis.

Injection of the cAMP-responsive element into the nucleus of Aplysia sensory neurons blocks long-term facilitation

IN both vertebrates and invertebrates, long-term memory differs from short-term in requiring protein synthesis during training1,2. Studies of the gill and siphon withdrawal reflex in Aplysia indicate

Coupling of hormonal stimulation and transcription via the cyclic AMP-responsive factor CREB is rate limited by nuclear entry of protein kinase A

Testing the hypothesis that the stoichiometry and kinetics of CREB phosphorylation are determined by the liberation and subsequent translocation of PKA catalytic subunit (C subunit) into the nucleus found that there was a linear relationship between the subsequent induction of the cAMP-responsive somatostatin gene and the degree ofCREBosphorylation.