IFIBYNE   05513
INSTITUTO DE FISIOLOGIA, BIOLOGIA MOLECULAR Y NEUROCIENCIAS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Pharmacological dissociation of memory expression and reactivation
Autor/es:
KARINA A. BARREIRO1, VICTORIA M. LYNCH1, LUIS D. SUÁREZ1, MARIANA FELD1, JOSÉ CLEMENTE1, VÍCTOR A. MOLINA AND ALEJANDRO DELORENZI
Lugar:
Cordoba
Reunión:
Congreso; SAN- Taller Argentino de Neurociencias 2012; 2012
Institución organizadora:
SAN
Resumen:
Cognition, Behavior, and MemoryPoster Number 59 / Session IIIPharmacological dissociation of memory expression andreactivationKarina A. Barreiro1, Victoria M. Lynch1, Luis D. Suárez1, Mariana Feld1, JoséClemente1, Víctor A. Molina2 and Alejandro Delorenzi1.1 Laboratorio de Neurobiología de la Memoria, Departamento de Fisiología yBiología Molecular y Celular, FCEyN, Universidad de Buenos Aires, IFIBYNECONICET,Argentina.2 Departamento de Farmacología, Facultad de Ciencias Químicas, UniversidadNacional de Córdoba, IFEC-CONICET, Argentina.k.barreiro@gmail.comIt was proposed by Tulving in 1983 that memories must be reactivated first, andthen a subsequent process would determine whether they can or cannot beexpressed. Reconsolidation approaches open the opportunity to explorewhether mechanisms mediating memory reactivation and those that underliebehavioral expression of memory can be dissociated. In the crabChasmagnathus memory model, animals associate the training context with avisual danger stimulus passing overhead. After a strong training protocol crabsexhibit long term memory 24–96 h later. In this model, a brief exposure (5minutes) to the training context (reminder) induces labilization andreconsolidation. We studied the effect of pre-reminder administration ofglutamate receptors AMPA and NMDA antagonist, CNQX and APVrespectively. We found that CNQX (1μg/g) did not impair the behavioralexpression of the memory but it did impair reconsolidation. Therefore, asexpected, the expressed memory became labile. In contrast, APV (1.5 μg/g)impaired behavioral expression of the memory but did not impair its ability to bereactivated. Hence, these findings suggest that NMDA receptor activation isrequired for memory expression but not for memory reactivation-labilization. Ourfindings show that when a memory is retrieved, the respective neuronal trace isreactivated although this trace may not take control over behavior