Biomedical subjects
Publications and source records attributed to D Quartermain.
Diethyldithiocarbamate, a dopamine beta hydroxylase inhibitor, decreases biosynthesis of norepinephrine in the brain. The effects of this inhibitor coincide with alterations in memory as demonstrated in single-trial passive avoidance in C57BL/6J mice.
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Retrograde amnesia for a passive avoidance response was produced in rats by electroconvulsive shock and in mice by cycloheximide, an inhibitor of protein synthesis. One day after training the memory could be restored if a "reminder" of the original foot shock was given after the retention test on which the amnesia was demonstrated. Memory did not return if the reminder was given without the prior retention test or if the reminder and the test were separated by 23 hours.
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Rats trained to press a bar for intracranial reinforcement gave as many responses during extinction as did water-reinforced controls, when extinction came immediately after an acquisition session. However, the experimental animals gave fewer responses in extinction than water-reinforced animals when extinction was delayed for 1 hour after acquisition. The activity level of the experimental animals was high immediately after acquisition but declined markedly over the delay period, which suggests that resistance to extinction after intracranial reinforcement is primarily a function of activity level.
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Rats were given a single electroconvulsive shock at varying intervals after receiving a punishing shock to the feet immediately after stepping into a compartment. Significant amounts of retrograde amnesia for the memory of the punishment was shown when electroconvulsive shock was administered up to and including 30 seconds after the punishment but not at 60 seconds. This brief temporal gradient cannot be explained in ternis of changed stimulus cues or learned interference analogouS to retroactive inhibition.
Pavlovian fear conditioning was employed to investigate learning during general anesthesia. Mice were given three CS-UCS presentations while anesthetized with halothane. The CS was a 10-s tone and the UCS a 0.4-mA shock delivered intramuscularly to the hindlimbs via needle electrodes. Anesthetized control groups received either CS only, UCS only, or CS followed by a 3-min delayed UCS. Strength of fear conditioning was assessed by measuring duration of suppression of drinking induced by tone presentation in a test session conducted 24 h after training. Results showed that mice trained under anesthesia exhibited a significant amount of conditioned suppression relative to the anesthetized control groups. These results show that Pavlovian fear conditioning can occur under halothane anesthesia.
The effects of stress on risk assessment behavior in mice were studied by examining latency to emerge from a safe compartment into a large, well-lit open field. In the first experiment different groups of mice were exposed for 1 h to tube restraint, fixed interval 2-min foot shock, or attack by an aggressive conspecific. Nonstressed controls were left undisturbed in the home cage. Thirty minutes following stress animals were placed in the safe compartment and latency to emerge was recorded. Results showed all of the stressed groups exhibited significantly faster emergence latencies than nonstressed controls. In the second experiment the duration of this effect was examined by testing different groups at varying intervals following tube restraint stress. Results showed that mice tested 0.5 and 1 h following stress exhibited short entry latencies and reduced head poke responses. Performance had returned to nonstress levels 3 h after stress. These data suggest that stress reduces caution by disrupting risk assessment behaviors.
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Noradrenergic and serotonergic systems are known to be stimulated during various forms of stress. The present study examined the effect of the beta-adrenergic serotonin1A receptor blocker propranolol on the ability of stress to elicit behavioral inhibition in mice. Mice were given the drug before immobilization or tube-restraint stress, and then were tested for either passive avoidance performance or time to emerge into an open field. Propranolol markedly potentiated stress-induced increases in latency in both of these tests, suggesting that it exacerbated reactions to stress. These results agree with previous data indicating that under certain conditions, propranolol can potentiate the effects of stress in rodents. The results support the hypothesis that the response of the noradrenergic and/or serotonergic systems to stress may have anxiolytic or antistress effects.