Sleep: changes in threshold to electroconvulsive shock in rats after deprivation of "paradoxical" phase

Rats were deprived of paradoxical (radid eye movement or REM) sleep for a 6-day period but were allowed substantial non-REM (slow wave) sleep. Thresholds for electroconvulsive shock dropped significantly after deprivation in all these animals, but thresholds in control animals treated in a similar manner, but allowed REM sleep exhibited no change. Deprivation seems to heighten neural excitability.     

Permanence of retrograde amnesia produced by electroconvulsive shock

The permanence of retrograde amnesia produced for a single training trial by a single electroconvulsive shock was studied. No recovery from amnesia was found with either single or repeated retention tests. Amnesic effects were found to be permanent with retention intervals as long as 1 month.     

Effect of electroconvulsive shock on an extinguished "fear" response

To test Gellhorn's hypothesis that electroconvulsive shock reinstates extinguished responses, a conditioned "anxiety" response was established and then extinguished in rats. A series of treatments did not restore the extinguished "anxiety" response; in fact, control animals showed appreciable spontaneous recovery of the "anxiety" response while treated animals did not.     

Licking rates of albino rats

Local licking rates of eight albino rats, when the rats were given tap water at the end of a short runway after 23 hours of water deprivation, averaged a little over seven licks per second. Small variations within sessions were found, rates being slightly but consistently higher at the beginning than later on in sessions. Inter-session and individual differences were also observed, but were only of theorder of one lick per second. Within practical limits, it appears that licking rates of rats are constant.     

Recovery of memory after amnesia induced by electroconvulsive shock

Electroconvulsive shock given to rats immediately after one-trial avoidance learning produced a significant amnesic effect 24 hours later; this amnesia had largely disappeared in further retention tests 48 and 72 hours after treatment. This result puts in question a basic assumption implicit in most memory consolidation studies that such amnesic effects will be permanent.     

Memory traces: experimental separation by cycloheximide and electroconvulsive shock

Mice given cycloheximide or saline were trained with a single trial. Electroconvulsive shock was administered to both groups at various times after training. Cycloheximide led to memory that decayed with time. Cycloheximide plus electroconvulsive shock produced complete amnesia at times when neither treatment alone produced amnesia. Only two types of processes appear to support memory storage in our study.     

Long-term analgesic effects of inescapable shock and learned helplessness

Although exposure to inescapable shocks induced analgesia in rats, the analgesia was not manifest 24 hours later. A brief reexposure to shock, however, restored the analgesia. This reexposure to shock had an analgesic effect only if the rats had been shocked 24 hours previously. Further, long-term analgesic effects depended on the controllability of the original shocks and not on shock exposure per se. Implications of these results for learned helplessness and stress-induced analgesia are discussed.     

Reinforcement magnitude as a determinant of performance decrement after electroconvulsive shock

The intensity of a foot shock may be a determinant of the rate at which an avoidance response becomes resistant to disruption by electroconvulsive shock. Mice were trained, one trial a day, in a passive avoidance learning task, with one of three foot-shock intensities. Electroconvulsive shock was administered at various intervals after each trial. At all foot-shock intensities, electroconvulsive shock given 10 seconds after each training trial was eflective in disrupting learning. Where electroconvulsive shock was given at longer intervals after each trial, those animals learning at low intensities of foot shock showed greater impairment of performance than those learning at high intensities.     

Sleep: the effect of electroconvulsive shock in cats deprived of REM sleep

Three cats were deprived of rapid-eye-movement (REM) sleep for 10 days, and three were deprived for 12 days. All cats received an electrically induced convulsion on each of the last 3 days of deprivation, as well as on the 1st recovery day just prior to sleep onset. As controls, four cats were deprived of REM sleep for 12 days and one was deprived for 10 days; the controls received no convulsions. Compensatory increases in REM sleep during recovery days were present in the convulsed animals, but were substantially lower than the recovery increases of control animals. During recovery REM sleep, convulsed cats did not display the exaggerated bursts of eye movements and body twitches seen in the nonconvulsed controls.     

Sleep: suppression of rapid eye movement phase in the cat after electroconvulsive shock

Electroconvulsive shock, administered for 5 to 7 days, reduced the daily rapid eye movement sleep time of seven cats to as little as 28 percent of base line levels. After day 4, eye movements during periods of cortical activation without tonic electromyographic activity were greatlyreduced. Although partially deprived of rapid eye movements for as long as 7 days, the cats showed no compensatory rise in rapid eye movement time during the recovery period, but controls equally deprived gave significant rebounds. Rapid eye movement time of anesthetized cats was not affected by current that usually produces con vulsions; it was lowered in animals convulsed with metrazol, but the same dosage of this drug, administered so as to avoid convulsions, had little eflect.It appears that some aspect of the convulsion is responsible for lowering the rapid eye movement time.     

Amnesia: a function of the temporal relation of footshock to electroconvulsive shock

When rats received a brief footshock upon stepping off an elevated platform, and an electroconvulsive shock 30 seconds or 6 hours afterward, amnesia was not observed 24 hours later. If a second footshock (noncontingent) was delivered 0.5 second before the electroconvulsive shock, amnesia was observed. The amnesia was temporary if conditioning was strong and permanent if conditioning was weak.     

Retrieval failure induced by electroconvulsive shock: reversal with dissimilar training and recovery agents

Amnesia was obtained following electroconvulsive shock in rats trained at one-trial passive avoidance of immersion in ice water. Avoidance behavior was restored when noncontingent foot shock was administered outside the training apparatus. The qualitative differences between ice water and foot shock demonstrate that the agent inducing recovery of memory need not be physically similar to the reinforcer used during training. These findings are interpreted as supporting a retrieval failure view of experimental amnesia.     

Retrograde amnesia produced by electroconvulsive shock after reactivation of a consolidated memory trace

Rats had a memory loss of a fear response when they received an electroconvulsive shock 24 hours after the fear-conditioning trial and preceded by a brief presentation of the conditioned stimulus. No such loss occurred when the conditioned stimulus was not presented. The memory loss in animals given electroconvulsive shock 24 hours after conditioning was, furthermore, as great as that displayed in animals given electroconvulsive shock immediately after conditioning. This result throws doubt on the assertion that electroconvulsive shock exerts a selective amnesic effect on recently acquired memories and thus that electroconvulsive shock produces amnesia solely through interference with memory trace consolidation.