A role for the Ras signalling pathway in synaptic transmission and long-term memory

Riccardo Brambilla, Nerina Gnesutta, Liliana Minichiello, Gail White, Alistair J. Roylance, Caroline E. Herron, Mark Ramsey, David P. Wolfer, Vincenzo Cestari, Clelia Rossi-Arnaud, Seth G. N. Grant, Paul F. Chapman, Hans-Peter Lipp, Emmapaola Sturani and Rdiger Klein ()
Additional contact information
Riccardo Brambilla: European Molecular Biology Laboratory
Nerina Gnesutta: Universita' di Milano
Liliana Minichiello: European Molecular Biology Laboratory
Gail White: Physiology Unit, School of Molecular and Medical Biosciences, University of Wales
Alistair J. Roylance: Centre for Genome Research, University of Edinburgh
Caroline E. Herron: Centre for Genome Research, University of Edinburgh
Mark Ramsey: Centre for Neuroscience, University of Edinburgh
David P. Wolfer: Anatomisches Institut, Universität Zürich
Vincenzo Cestari: Istituto di Psicobiologia e Psicofarmacologia del Consiglio Nazionale delle Ricerche
Clelia Rossi-Arnaud: Universita' di Roma La Sapienza
Seth G. N. Grant: Centre for Genome Research, University of Edinburgh
Paul F. Chapman: Physiology Unit, School of Molecular and Medical Biosciences, University of Wales
Hans-Peter Lipp: Anatomisches Institut, Universität Zürich
Emmapaola Sturani: Universita' di Milano
Rdiger Klein: European Molecular Biology Laboratory

Nature, 1997, vol. 390, issue 6657, 281-286

Abstract: Abstract Members of the Ras subfamily of small guanine-nucleotide-binding proteins are essential for controlling normal and malignant cell proliferation as well as cell differentiation1. The neuronal-specific guanine-nucleotide-exchange factor, Ras-GRF/CDC25Mm (refs 2,3,4), induces Ras signalling in response to Ca2+ influx5 and activation of G-protein-coupled receptors in vitro6, suggesting that it plays a role in neurotransmission and plasticity in vivo7. Here we report that mice lacking Ras-GRF are impaired in the process of memory consolidation, as revealed by emotional conditioning tasks that require the function of the amygdala; learning and short-term memory are intact. Electrophysiological measurements in the basolateral amygdala reveal that long-term plasticity is abnormal in mutant mice. In contrast, Ras-GRF mutants do not reveal major deficits in spatial learning tasks such as the Morris water maze, a test that requires hippocampal function. Consistent with apparently normal hippocampal functions, Ras-GRF mutants show normal NMDA (N-methyl-D-aspartate) receptor-dependent long-term potentiation in this structure. These results implicate Ras-GRF signalling via the Ras/MAP kinase pathway in synaptic events leading to formation of long-term memories.

Date: 1997
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DOI: 10.1038/36849

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