IFEC   20925
INSTITUTO DE FARMACOLOGIA EXPERIMENTAL DE CORDOBA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Molecular mechanisms underlying promotor effect of IGF-1 on the formation of a fear memory trace
Autor/es:
ESPEJO PABLO JAVIER; CALFA GASTION DIEGO; HERRERA MACARENA LORENA; COMAS MUTIS RAMIRO GABRIEL; HEREÑÚ CLAUDIA BEATRIZ; CHAMPARINI LEANDRO GABRIEL; OTAMENDI ANDREA; MOLINA VICTOR ALEJANDRO
Lugar:
Carlos Paz
Reunión:
Congreso; XXXIV Reunión Anual de la Sociedad Argentina de Investigacion en Neurociencias; 2019
Institución organizadora:
Sociedad Argentina de Investigación en Neurociencias
Resumen:
Basolateral amygdala complex (BLA) plays an essential role in the generation of an emotional state caused by an aversive experience. Insulin like growth factor 1 (IGF-1) could modulate hippocampal circuits modifying cognitive functions, and possibly, the molecular mechanisms involved in some psychopathologies related to traumatic memories.Objective To evaluate the formation of a memory trace through BLA IGF-1 gene therapy and synaptic and molecular changes in dorsal hippocampus (HD) and BLA associated with the formation of this memory trace.M&M: Adult male Wistar rats were bilaterally infused into BLA with RAd-IGF1, and RAd-DsRed as control. 7 days later we performed a weak fear conditioning protocol (WFCP). Freezing behavior (FB) was assessed at 7th and 14th day. HD synaptic plasticity was assesed through dendritic spine analysis. BLA and HD were obtained for protein analysis.Results: A significantly increase in FB in the RAd-IGF1 group was observed after 7 days and 14 days post injection. There was a significant increase in mature spines after RAd-IGF1 treatment. pERK/ERKt level was increased in BLA in RAd-IGF1 group at the time WFCP was performed.Conclusions: IGF-1 gene therapy induces a significant expression of FB in a WFCP, with a possible promotor effect on the formation of a fear memory trace. This behavioral expression was coincident with changes in HD dendritic plasticity. This effect could be partially attributed to MAPK/ERK pathway activation in BLA.