Labilize or not labilize? That is the question

M.S. FUSTIÑANA; V. DE LA FUENTE; R.A.M. FREUDENTHAL; A. ROMANO

Florencia

Congreso; 8 th IBRO World Congress of Neuroscience; 2011

IBRO

Once a memory is consolidated, the presentation of a reminder can induce reconsolidation, a process that has inherent stages:reactivation, labilización and restabilization of the memory trace. We are studying the labilization process in two contextual associative modelsin phylogeneticaly distant species: context-signal memory in the crab Chasmagnathus and fear conditioning in mouse.We analysed the role of the proteasome system in memory labilization. A previous study indicated that the labilization process involvedprotein degradation by the proteasome. Here we found that the inhibition of the proteasome system by MG132 block labilization. Ourlaboratory had shown that this drug is capable to inhibit NF-kB during consolidation and the inhibition of this transcription factor results inan amnesic effect. Paradoxically, when we administered MG132 previous the re-exposure we did not find an amnesic effect onmemory reconsolidation. However, when we co-injected this proteasoma inhibitor with sulfasalazine (a NF-kB inhibitor) we could not findthe amnesic effect we used to obtain after sulfasalazine administration previous to the reexposure. It had been demonstrated that bicuculline,a GABA inhibitor can facilitate memory reconsolidation in the crab paradigm. Hence we co-injected bicuculline with MG132 and wewere incapable to facilitate memory reconsolidation. When we co-administered MK801, a NMDA receptor inhibitor with MG132, we also coudnot find the amnesic effect of MK801. All together these results indicate that proteasoma is involved in memory labilization. Thehypothesis underlying is that memory labilization implies at least partial synapses retraction involving proteasoma dependent proteindegradation and then stabilization during the reconsolidation process.