Muscarinic antagonism during consolidation disrupts long-term memory expression without affecting memory storage

. LUIS DANIEL SUÁREZ; PEDRO CAFFARO, KARINA A. BARREIRO MARIANO G. BLAKE Y ALEJANDRO DELORENZI

Cordoba

Congreso; SAN- Taller Argentino de Neurociencias 2012; 2012

SAN

Cognition, Behavior, and MemoryPoster Number 116 / Session IIIMuscarinic antagonism during consolidation disrupts long-termmemory expression without affecting memory storageLuis Daniel Suárez 1, Pedro Caffaro 1, Karina Andrea Barreiro 1, Mariano Blake2, Alejandro Delorenzi 11 Laboratorio de Neurobiología de la Memoria – Facultad de Ciencias Exactas yNaturales, UBA – IFIBYNE - CONICET2 Laboratorio de Neurofarmacología de los Procesos de Memoria – Facultad deFarmacia y Bioquímica, UBAlsuarez@fbmc.fcen.uba.arUntil now, most works on induced amnesia in animal models interpreted deficitsin memory expression as deficits in the storage or retrieval of memory. Weproposed that during consolidation, acquired information is evaluated and thatduring this process it is decided whether the new memory is going to beexpressed or not in the long-term. A protocol to test whether a non-expressedmemory trace is indeed an intact functional memory that can be retrieved -evenwhen is not expressed- is to prove that this memory is able to enter inreconsolidation. For this purpose, a reminder is presented followed by afacilitatory treatment that changes long-term memory expression. Very acutecontrols for memory reconsolidation are needed to discard another effectsrelated to reminder presentation, as summation of new memories. We foundthat the amnesic effect of pre- and post-training scopolamine (SCP, acompetitive muscarinic receptor blocker) injections can be reversed byimproving memory reconsolidation. This reversion depends not only in thepresentation of a reminder, but also this reminder must be able to triggerreconsolidation, thus ruling out summation effects. On the contrary, higherdoses of SCP or sulfazalazine (that induces amnesia by reducing the entranceto the nucleus of NF-B transcription factor) induce amnesias that can not bereverted by this protocol, thus showing that storage of memory or the formationof retrieval links could have been disrupted by those treatments