DE OLMOS SOLEDAD
Congresos y reuniones científicas
Título:
Differential activation of the subdivisions of retrosplenial cortex associated to the retrieval of fear conditioned memory
Autor/es:
SIGWALD ERIC LUCA; PONCE NICOLAS; BIGNANTE ANALIA; MOLINA VICTOR; DE OLMOS SOLEDAD; LORENZO ALFREDO
Lugar:
Puerto Varas
Reunión:
Congreso; Chilean society for cell biology XXX Annual Meeting; 2016
Institución organizadora:
Chilean society for cell biology
Resumen:
Introduction: The retrosplenial cortex (RSC) has been implicated in complex cognitive functions such as learning, memory, spatial navigation and introspection. Dysfunction of RSC is associated with diverse pathological conditions such as Alzheimer´s disease, autism or schizophrenia. Thus, addressing the functional organization and activity of the subdivisions of RSC (areas A29 and A30) during the execution of complex cognitive tasks might be relevant for understanding their physiological and pathological roles.Material and Methods: Immunostaining was used for a comprehensive analysis of cFos and EGR-1 expression in RSC and related areas of male rats after acquisition and retrieval of contextual fear memory. The impact of MK801 treatment that selectively induces degeneration of layers IV-V neurons of A29 (A29MK801) was evaluated.Results: Acquisition and evocation of fear memory promoted the expression of cFos and EGR-1 in A30, dorsal hippocampus (DH), medial entorhinal cortex (MEnt) and basolateral amygdala (BLA) while EGR-1 expression was down-regulated in A29 and caudomedial entorhinal cortex (CEnt). After fear conditioning, selective degeneration of A29MK801 neurons impaired fear memory retrieval and prevented cFos and EGR-1 up-regulation in A30, without affecting their expression in DH, MEnt, BLA and CEnt. Discussion: These observations indicated that RSC integrity is required for fear memory retrieval. The data also showed that fear memory evocation elicits differential neuronal activation in RSC subdivisions, suggesting that A30 activation depends on the functional integrity of A29MK801 neurons.