Evidence that protein synthesis inhibitors induce amnesia in a variety of species and learning paradigms indicates that the consolidation of newly acquired information into stable memories requires the synthesis of new proteins.
Because extinction of a response also requires acquisition of new information, extinction, like original learning, would be expected to require protein synthesis.
In this and following figures, retrieval values are expressed as median (interquartile range) step-down latency, in seconds. In the experiments shown in this figure, unoperated animals were used.
On the test sessions the foot-shock (US) was not administered.
The difference in step-down latency between the training session and the 1st test session was used as a measure of retention (i.e., retrieval) of the learned response (5, 6, 12, 18, 19). 1 Repeated exposure to the training apparatus without reinforcement induces extinction of one-trial avoidance.
The present experiments examined the involvement of protein synthesis in the hippocampus of rats in the learning and extinction of one-trial inhibitory avoidance, a form of contextual fear conditioning used extensively in studies of the pharmacology and biochemistry of memory consolidation (6, 7).
The learning of this task is known to require hippocampal protein synthesis (12).
The present experiments examined the involvement of protein synthesis in the hippocampus in the extinction of a learned fear-based response known to involve the hippocampus.
Rats were trained in a one-trial inhibitory avoidance task in which they received footshock after stepping from a small platform to a grid floor.
Male Wistar rats (age, 2–3 months, weight, 220–260 g) were used.
The animals were housed in plastic cages, five to a cage, with water and food available ad libitum, under a 12-h light/dark cycle (lights on at a.m.) at a constant temperature of 23°C.
The -aspartate (NMDA) antagonist APV blocks the consolidation of many tasks (5–8) and also blocks both the consolidation (5) and the extinction of conditioned fear tasks (9).
Recent findings indicate that infusions of the protein synthesis inhibitor anisomycin or the β-adrenoreceptor antagonist propranolol administered into the insular cortex block both the consolidation (10) and the extinction of conditioned taste aversion (11).
These findings are consistent with other evidence that anisomycin blocks both the consolidation of original learning and extinction.