D-055 | ERK regulatory mechanisms in memory and plasticity.

Cognition, Behavior, and Memory
Author: Santiago Ojea Ramos | Email: ojea.santiago@gmail.com

Santiago Ojea Ramos^1°, Candela Medina^2°, María del Carmen Krawczyk^2°,  Millán Julieta^2°, Acutain María Florencia^3°, Báez María Verónica^3°, Urbano Suarez Francisco José^1°,  Romano Arturo Gabriel^1°, Boccia Mariano Martin^2°, Feld Mariana^1°

^1° Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), UBA-CONICET.
^2° Laboratorio de Neurofarmacología de Procesos de Memoria, Cátedra de Farmacología, Facultad de Farmacia y Bioquímica – UBA.
^3° Instituto de Biología Celular y Neurociencias Prof. Dr. E. de Robertis (IBCN), CONICET-UBA

Extensive research has focused on ERK1/2 phosphorylation in memory and plasticity, while other regulatory mechanisms remain mostly unexplored. Here, we present findings on two less-studied regulatory mechanisms: ERK2 dimerization (a post-translational modification affecting interaction with cytosolic targets), and the role of MAPK phosphatase 3 (MKP-3, also known as DUSP6), a cytosolic negative regulator of the pathway.
We assessed ERK2 dimerization during chemical long-term potentiation (cLTP) in mature rat primary cortical neuronal cultures, as well as in mice hippocampus after inhibitory avoidance (IA) memory reactivation. We also studied the impact of DEL-22379 (DEL), a specific ERK dimerization inhibitor on LTP induced in hippocampal slices (LTP), cLTP and memory reconsolidation.
In parallel, we also determined MKP-3 expression levels and the effect of inhibiting it (with BCI, its specific inhibitor) during IA reconsolidation.
Our results suggest a pivotal role of ERK2 dimerization and MKP-3 in plasticity and IA memory reconsolidation, but deserve further research.
This is the first study to document ERK dimerization in neural tissue and its impact on these processes.