Drug induced retrograde amnesia.
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Mice were tested in a situation permitting them to step readily from a small, restrictive platform to a larger one. Conditioned avoidance was established by a single training trial when animals received a shock by stepping from one platform to another. At various intervals after the single punishing shock, subjects were anesthetized with diethyl ether. Interference with retention, tested 1 day later, was shown for intervals up to 24 minutes, at which time ether no longer appeared to influence the subsequent response.
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Emotional responses such as fear are rapidly acquired through classical conditioning. This report examines the neural substrate underlying memory of acquired fear. Rats were classically conditioned to fear both tone and context through the use of aversive foot shocks. Lesions were made in the hippocampus either 1, 7, 14, or 28 days after training. Contextual fear was abolished in the rats that received lesions 1 day after fear conditioning. However, rats for which the interval between learning and hippocampal lesions was longer retained significant contextual fear memory. In the same animals, lesions did not affect fear response to the tone at any time. These results indicate that fear memory is not a single process and that the hippocampus may have a time-limited role in associative fear memories evoked by polymodal (contextual) but not unimodal (tone) sensory stimuli.
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Old memory, when reactivated by cue exposure, was disrupted by mild or deep hypothermia treatments. New memory was impaired only by deep cooling. Moreover, old but not new learning showed spontaneous recovery. Old reactivated memory may be qualitatively different from newly acquired memory.
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Bromolysergide (BOL 148) and methysergide (UML 491), 2 mg/kg intraperitoneally, and saline were administered to rats 45 min before one-trial passive-avoidance conditioning followed by electroconvulsive shock (ECS) or sham-ECS (ECS). On test session (24 h later), the groups treated with both BOL 148 and UML 491 exhibited a clear-cut retention in comparison to saline-ECS rats. On the other hand, all drugged groups, regardless of their submission to ECS, showed a little less pronounced consolidation than saline-ECS rats. The antiamnestic effect brought about by the two drugs was discussed in terms of receptor antagonism against ECS-released brain serotonin, whereas the lower passive-avoidance level observed in treated animals was considered in relation to a possible antipunishment effect of antiserotoninergic treatment.
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