Memory reacquisition deficit: Chicks fail to relearn pharmacologically disrupted associative response.

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.