Author:
Wood Marcelo A.,Kaplan Michael P.,Park Alice,Blanchard Edward J.,Oliveira Ana M.M.,Lombardi Thomas L.,Abel Ted
Abstract
Deletions, translocations, or point mutations in the CREB-binding protein
(CBP) gene have been associated with Rubinstein-Taybi Syndrome; a human
developmental disorder characterized by retarded growth and reduced mental
function. To examine the role of CBP in memory, transgenic mice were generated
in which the CaMKIIα promoter drives expression of an inhibitory
truncated CBP protein in forebrain neurons. Examination of hippocampal
long-term potentiation (LTP), a form of synaptic plasticity thought to
underlie memory storage, revealed significantly reduced late-phase LTP induced
by dopamine-regulated potentiation in hippocampal slices from CBP transgenic
mice. However, four-train induced late-phase LTP is normal. Behaviorally, CBP
transgenic mice exhibited memory deficits in spatial learning in the Morris
water maze and deficits in long-term memory for contextual fear conditioning,
two hippocampus-dependent tasks. Together, these results demonstrate that CBP
is involved in specific forms of hippocampal synaptic plasticity and
hippocampus-dependent long-term memory formation.
Publisher
Cold Spring Harbor Laboratory
Subject
Cellular and Molecular Neuroscience,Cognitive Neuroscience,Neuropsychology and Physiological Psychology
Cited by
292 articles.
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