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Effects of increasing CREB‐dependent transcription on the storage and recall processes in a hippocampal CA1 microcircuit
Author(s) -
Bianchi Daniela,
Michele Pasquale De,
Marchetti Cristina,
Tirozzi Brunello,
Cuomo Salvatore,
Marie Hélène,
Migliore Michele
Publication year - 2014
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.22212
Subject(s) - creb , hippocampal formation , neuroscience , neuronal memory allocation , recall , long term potentiation , hippocampus , psychology , biology , transcription factor , medicine , receptor , cognitive psychology , excitatory postsynaptic potential , inhibitory postsynaptic potential , biochemistry , gene , synaptic fatigue
The involvement of the hippocampus in learning processes and major brain diseases makes it an ideal candidate to investigate possible ways to devise effective therapies for memory‐related pathologies like Alzheimer's Disease (AD). It has been previously reported that augmenting CREB activity increases the synaptic Long‐Term Potentiation (LTP) magnitude in CA1 pyramidal neurons and their intrinsic excitability in healthy rodents. It has also been suggested that hippocampal CREB signaling is likely to be down‐regulated during AD, possibly degrading memory functions. Therefore, the concept of CREB‐based memory enhancers, i.e. drugs that would boost memory by activation of CREB, has emerged. Here, using a model of a CA1 microcircuit, we investigate whether hippocampal CA1 pyramidal neuron properties altered by increasing CREB activity may contribute to improve memory storage and recall. With a set of patterns presented to a network, we find that the pattern recall quality under AD‐like conditions is significantly better when boosting CREB function with respect to control. The results are robust and consistent upon increasing the synaptic damage expected by AD progression, supporting the idea that the use of CREB‐based therapies could provide a new approach to treat AD. © 2013 Wiley Periodicals, Inc.