Cognition, Behavior, and Memory
Author: Matias Martìn Renfijes | Email: firstname.lastname@example.org
Matias Martìn Renfijes 1°3°, Juan Gabriel Riboldi 1°3°, Julieta Andrea Corrales 1°3°, Haydee Ana Marìa Viola 1°2°3°
1° Facultad de Medicina. Universidad de Buenos Aires. Buenos Aires, Argentina. Laboratorio de Memoria, Instituto de Biología Celular y Neurociencias “Prof. E. De Robertis” (IBCN), Facultad de Medicina, UBA-CONICET, Buenos Aires, Argentina.
2° Departamento de Fisiología, Biología Molecular y Celular “Dr. Héctor Maldonado” (FBMC), Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina.
3° Laboratorio de Bioingeniería, Departamento de Ciencias de la Vida, Instituto Tecnológico de Buenos Aires
One of the functions of astrocytes is to control the permanence of glutamate in the synaptic space, exerted by specific transporters expressed throughout the brain. Here we studied the role of the glutamate transporter GLT-1, specifically located in astrocytes, in the consolidation, expression and reconsolidation of Contextual Fear Conditioning (CFC) memory. Dihydrokainic acid (DHK), a selective GLT-1 inhibitor, was infused into the rat hippocampus in order to affect different stages of memory. We observed that DHK administration around conditioning did not affect long term memory (LTM) consolidation induced by a strong training session. However, short-term memory (STM) or LTM expression was impaired when DHK was administered 15 min before test sessions. Also, if applied 15 minutes after a reactivation session, DHK impaired memory reconsolidation. In contrast, after a weak training session, which only induced STM, hippocampal inhibition of GLT-1 showed a promotion of LTM formation. In conclusion, we found that GLT-1 blockade close to training time helps to consolidate CFC memory induced by weak training but not by strong training. However, the blockade of this transporter also interferes with memory expression and reconsolidation. We describe the complete dynamics of an aversive memory under the hippocampal effects of astroglial glutamate reuptake blockade, being a site of action for the development of new post-traumatic stress and cognitive impairment treatments.