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Laboratorio de Neurobiología de la Memoria, Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires. IFIByNE, CONICET. Ciudad Universitaria, Pab. II, 2do piso (1428EHA). Buenos Aires, Argentina
* To whom correspondence should be addressed. E-mail: aromano{at}fbmc.fcen.uba.ar
Consolidation of long-term memory requires the activation of several transduction pathways that lead to post-translational modifications of synaptic proteins and to regulation of gene expression, both of which promote stabilization of specific changes in the activated circuits. In search of the molecular mechanisms involved in such processes, we used the context-signal associative learning paradigm of the crab Chasmagnathus. In this model, we studied the role of some molecular mechanisms, namely cAMP-dependent protein kinase (PKA), extracellular-signal-regulated kinase (ERK), the nuclear factor kappa B (NF-
B) transcription factor, and the role of synaptic proteins such as amyloid ß precursor protein, with the object of describing key mechanisms involved in memory processing. In this article we review the most salient results obtained over a decade of research in this memory model.
Abbreviations: APP, amyloid precursor protein CSM, context-signal memory ERK, extracellular-signal-regulated kinase ITI, intertrial interval JNK, c-Jun N-terminal kinase LTM, long-term memory MAPK, mitogen-activated protein kinase NF-
B, nuclear factor kappa B NF, natural fibril PKA, protein kinase A TF, transcription factor
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