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| Research article summary (published 30 Jan 2003): |
Signaling from cAMP/PKA to MAPK and synaptic plasticity.
Full Abstract
The facilitation of hippocampus-based, long-lasting synaptic plasticity, which is frequently investigated in model systems such as long-term potentiation (LTP) and in learning paradigms such as the Morris water maze, is associated with several cellular key events:
Ca(2+) influx through the N-methyl-D-aspartate (NMDA) receptor, generation of cyclic AMP (cAMP) and activation of protein kinase A (PKA), phosphorylation of mitogen-associated protein kinase (MAPK) and cAMP-response element-binding protein (CREB), and subsequent transcription of plasticity-associated genes. Recently, a signal-transduction cascade from cAMP/PKA to MAPK was discovered, which seems to be neuron-specific and comprises the critical events of hippocampus-based long-term plasticity described here into one single cascade. A major alternative to cAMP/PKA-MAPK signaling are the cascades from Ca(2+) to MAPK via Ras. However, Ras is inhibited by PKA. This article reviews the studies that argue for the existence of two competing pathways, and discusses their implication for the molecular mechanisms underlying synaptic plasticity.
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Author information
Author/s: Waltereit, Robert (R); Weller, Michael (M);
Affiliation: Department of Neurology, University of Tübingen, Germany. robert.waltereit(-atsign-)uni-tuebingen.de
Journal and publication information
Publication Type: Journal Article; Review
Journal: Molecular neurobiology (Mol Neurobiol), published in United States. (Language: eng)
Reference: 2003-Feb; vol 27 (issue 1) : pp 99-106
Dates: Created 2003/04/01; Completed 2003/05/30; Revised 2007/11/15;
PMID: 12668903, status: MEDLINE (last retrieval date: 11/6/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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