New memories are stabilized after a learning experience by a process called consolidation. Memories are not consolidated forever: retrieval of consolidated memory can induce a labile phase during which memory could be disrupted or reconsolidated. Reconsolidation is the hypothetical process that is reactivated after memory retrieval. Recent studies have shown that reconsolidation could be disrupted acting on specific molecular levels (i.e. glutamatergic system). There is strong evidence that Pavlovian fear memories undergo reconsolidation and it was proposed that interventions to disrupt reconsolidation may help for specific and selective inhibition of fear related memories and, similarly, appetitive memories (i.e. for drug addiction). However it is not known if all memories or if only certain kind of memories could be retrieved and reconsolidated or disrupted. To date reconsolidation of instrumental learning memories is under discussion. Aim of this study is to investigate if it is possible to disrupt nicotine- related instrumental learning memories reconsolidation. The experimental paradigm is operant conditioning and the model used is intravenous nicotine self-administration (S/A). Rats were trained to nicotine S/A without Pavlovian association to visual cues (CS). We tested the occurrence of instrumental learning reconsolidation through its absence after pharmacological treatments aimed to disrupt it, such as antagonism of NMDA receptors with MK-801. Instrumental learning reconsolidation disruption was tested after 10 days of training, 14 days of forced abstinence (rats kept in their home cages) and retrieval of instrumental learning to operant levers without consequences upon responding, followed by MK-801 or saline treatment. Day after test of renewal showed that re-exposure to 20, but not 2, active lever pressings in the operant chamber at retrieval was able to induce 24 hours later a spontaneous recovery inhibited by MK-801. Taken together, the experimental design (training, retrieval and spontaneous recovery in the same context) and the significant difference between saline and MK-801 treatment before re-exposure to 20 active lever presses suggest that the absence of spontaneous recovery is due to instrumental memory reconsolidation disruption and not extinction. However a molecular approach in support of the behavioural data is needed in order to determine the increase of molecular markers correlating reconsolidation (e.g., Zif-268).
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