Samenvatting

Addiction is known for the craving effects that the drug of abuse has on the addicted. It has been shown that conditioned associations between the effects of an addictive drug and environmental stimuli play an important role in the maintenance of drug self-administration. When memories are gained they initially persist in a fragile state and are transformed into stable memories over time. This formation of memory is called consolidation. The consolidation hypothesis suggests that processes underlying new memories initially persist in a fragile state and consolidate over time. Consolidation of new memory requires protein synthesis. Recent evidence suggests that the re-activation of old memory or retrieval, turns this memory back into an unstable memory, which needs to be re-formed; this re-forming of old memory is called reconsolidation. So is reconsolidation another round of consolidation? The answer is no, because consolidation and reconsolidation do share common molecular mechanisms, but they are distinct processes because they require, with some degree of overlap, the activation of different brain areas and circuits. In previous research it has been shown that reconsolidation is mediated, for some paradigms, by the basolateral amygdala (BLA). Moreover in several addiction studies, it has been shown that the memory for the learned task can be disrupted. This reports fits in with these studies. However the experiments that were performed in this report were related to the self-administration of the drug of abuse. We report that BLA infusions with anisomycin, a protein synthesis inhibitor, did not impair the reconsolidation of self-administration memory of sucrose during the first reconsolidation of memory. However further research is necessary. Rats were trained to self-administer sucrose and after three weeks they were infused with either anisomycin or saline immediately after re-exposure to the self-administration environment. The following day nose-poking behaviour was determined. Nose-poking behaviour was used as an index of memory reconsolidation. Moreover, there is evidence that the noradrenergic system is involved in reconsolidation, more specific the ß-adrenoreceptor. We report that injection of propranolol, a ß-adrenoreceptor antagonist, disrupts the reconsolidation of self-administration memory of sucrose. Rats were trained in the same way as the previous experiment. In a second experiment they were re-trained to demonstrate whether propranolol disrupts the re-learning of self-administrating of sucrose. It demonstrates that there was no disruption of the long-term memory. Following training the rats again underwent the training session, the re-exposure and the test. However during the re-exposure they were subjected to the cues that were paired to the sucrose delivery and sucrose availability, in order to determine the potency of cues on reconsolidation. As in the first experiment propranolol injection didn’t affect nose-poke behaviour three weeks after training, but was able to disrupt reconsolidation four weeks post training.