CONICET | Buscador de Institutos y Recursos Humanos

When a well-consolidated memory is recalled it becomes transiently sensitive to disruption to the same treatments that affect consolidation. This new window of susceptibility is referred as memory reconsolidation. Here we investigate the effect of nicotinic receptor (nAchR) ligands infused bilaterally in the dorsal hippocampus after memory reactivation of the inhibitory avoidance response in mice. The nAchR antagonists were mecamylamine (MEC, α3β4, 1-30 ug/side), dihydro-β-eritroidine (DHβE, α4β2 , 330 ug/side) and methyllycaconitine (MLA, α7,1-30 ug/side). Mice that were over-reinforced (1.2 mA, 50 Hz, 1 s) on the learning trial, exhibited a high retention performance 48 h after training. The immediate intrahippocampal infusion of MEC, DHβE or MLA after the retention test, that is, after memory reactivation, significantly impaired retention performance in a dose- and time-dependent manner. When memory was retrieved 48 h training and the drugs were given immediately after it, spontaneous recovery was not observed in a new retrieval session 21 days after original learning. Although we cannot definitively discard a retrieval deficit, the results obtained are in accordance with the storage deficit interpretation. Retention performance was unchanged in drugs - treated mice not undergoing memory reactivation session. These results, taken together, indicate that different nicotinic antagonists impaired reconsolidation of an inhibitory avoidance task in mice, suggesting a critical participation of the cholinergic nicotinic pathway in this memory processes.

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