In search of the mechanisms that differentially determine long-term memory storage and expression

LUIS DANIEL SUÁREZ; PEDRO CAFFARO; LIA FRENKEL; VERÓNICA COCCOZ; MARIANO BLAKE; FERNANDO LOCATELLI; HÉCTOR MALDONADO; ALEJANDRO DELORENZI

Huerta Grande, Córdoba

Congreso; I Reunión Conjunta en Neurociencias (IRCN); 2009

Taller Argentino de Neurociencias (TAN) y Sociedad Argentina de Investigaciones en Neurociencias (SAN)

<!-- /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin:0cm; margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-fareast-font-family:"Times New Roman";} @page Section1 {size:612.0pt 792.0pt; margin:70.85pt 3.0cm 70.85pt 3.0cm; mso-header-margin:36.0pt; mso-footer-margin:36.0pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> In search of the mechanisms that differentially determine long-term memory storage and expression Suárez, Luis D.; Caffaro, Pedro; Frenkel, Lia; Coccoz, Verónica; Locatelli, Fernando; Maldonado, Héctor and Delorenzi, Alejandro Laboratorio de Neurobiología de la Memoria – Facultad de Ciencias Exactas y Naturales, UBA – IFIBYNE - CONICET Not every acquired experience builds a memory that can be expressed in the long term. Until now, deficits in memory expression were interpreted as deficits in memory storage, or in retrieval. However, evidence in the crab Chasmagnathus, and very recently in humans, have shown that encoded memory traces can be retrieved even in the absence of behavioral expression. This fact implies that the mechanisms involved in expression and storage of long-term memory are different. Our main goal is studying the mechanisms that determine during consolidation whether a memory trace will be behaviorally expressed on the long term. In this framework, we propose that to reopen the possibility for neuromodulators to improve memory expression is a functional value of reconsolidation. A first approach to this problem is to isolate the treatments that induce deficits in memory expression from those that induce “true amnesia”. The basic behavioral protocol consists in the interference of memory consolidation followed by a subsequent post-reminder facilitator treatment. Under this circumstance, if memory expression is reinstalled after facilitation of reconsolidation, the mechanism interfered should be related to memory expression and not to memory storage. Angiotensin II is a neuromodulator that affects long-term memory expression. As other systems should be involved, initially we will study glutamatergic and muscarinic neurotransmission during acquisition and during consolidation, as well as NF-kB transcription factor. In order to understand at cellular level the processes involved in long-term memory expression, neurons and neuropils related to memory process will be studied both by in vivo neuroimaging and by markers of neuronal activity.