ABSTRACT
It is generally assumed that if memory is disrupted by pharmacological inhibitors during its consolidation, it can be later acquired afresh. In our experiments, we trained day-old chicks in a one-trial passive avoidance task and interfered with memory formation using protein synthesis inhibitor anisomycin or NMDA receptor antagonist MK-801. Second training was then given to amnestic animals with either the same conditioning stimulus (retraining) or a new one (novel training). Retraining with the same stimulus failed to produce efficient memory at all the examined between-training and training-to-test intervals, while a new conditioned stimulus was learned successfully. We suggest that this memory reacquisition deficit may result from the failure of associative memory co-allocation mechanisms.
