Anticholinesterase-induced amnesia and its temporal aspects

Injection of the anticholinesterase drug diisopropyl fluorophosphate into the hippocampi of rats, 30 minutes after escape learning, produces partial amnesia with full recovery 5 days after injection. No such amnesia is produced if the injection takes place 3 days after learning. However, with injections 5 days after learning there is again an effect, and at 14 days amnesia is complete though no normal forgetting occurs within this period.     

Amnesia produced by electroconvulsive shock or cycloheximide: conditions for recovery

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.     

Effects of Electroshock on Memory: Amnesia without Convulsions

Mice received a single training trial on an inhibitory avoidance task and a retention trial 24 hours later. Electroshock stimulation, administered 25 seconds after the training trial, produced amnesia even if the convulsion was prevented by ether anesthesia. The amnesia produced by such shock is apparently due to the electric current and not to the convulsion.     

Retrograde amnesia gradients: effects of direct cortical stimulation

Electrical stimulation was delivered bilaterally to either the anterior or posterior cortex in rats from 0.1 second to 4 hours after a single training trial on an inhibitory avoidance task. As indicated by a retention test given 24 hours later, the length of the retrograde amnesia gradients ranged from 5 seconds to 240 minutes, depending on the brain region stimulated and the intensity of the stimulating current. The stimulation intensity that was threshold for amnesia varied directly with the length of the interval between training and treatment.     

Histamine: effect on self-stimulation

When injected discretely into the lateral hypothalamus of rats, histamine inhibited electrical self-stimulation at the injection site without affecting self-stimulation in the contralateral lateral hypothalamus. This effect was blocked by prior treatment with antihistaminics. Histidine, the amino acid precursor of histamine, produced a similar effect after a delay of 6 to 10 minutes.     

Retrograde amnesia: electroconvulsive shock effects after termination of rapid eye movement sleep deprivation

Mice that were deprived of rapid eye movement sleep for 2 days immediately after one-trial training in an inhibitory avoidance task and were given an electroconvulsive shock after deprivation displayed retrograde amnesia on a retention test given 24 hours later. Electroconvulsive shock produced no amnesia in comparable groups of animals that were not deprived of rapid eye movement sleep.     

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.     

Long temporal gradient of retrograde amnesia for a well-discriminated stimulus

This experiment tested the general validity of recent findings that retrograde amnesia can be produced by electroconvulsive shock only if the shock is administered within 10 to 30 seconds after the learning trial. Precautions were taken to avoid confusion of other shock effects with retrograde amnesia. A temporal gradient of elec- troconvulsive shock-produced retrograde amnesia, extending up to at least 1 hour, for a well-discriminated stimulus, was demonstrated in mice in a one-trial learning passive avoidance situation.     

Memory: modification of anisomycin-induced amnesia by stimulants and depressants

Mice were trained in a passive (foot shock)avoidance task. When administered after training, the stimulants caffeine or nicotine blocked amnesia for the task that had been produced by injections of the protein synthesis inhibitor anisomycin given prior to training. With foot shock at a higher intensity, anisomycin did not produce amnesia by itself, but the administration of the depressants chloral hydrate or sodium phenobarbital after training did cause amnesia. Stimulants and depressants did not have an appreciable influence on the overall degree of protein synthesis inhibition produced by anisomycin. The results support the hypothesis that arousal after training is an important factor in the conversion of short-term to long-term memory.     

Amnesia or reversal of forgetting by anticholinesterase, depending simply on time of injection

The effect of intracerebral injections of the anticholinesterase drug diisopropyl fluorophosphate in rats was to produce good recall of an otherwise almost forgotten habit learned 28 days before. The same injections produced temporary amnesia for the same habit, otherwise well remembered, learned 14 days before. The injections had no ef fect on the memory of the same habit when it was only partly learned 14 days before. The results support the hy pothesis that the physiological basis of memory lies in an increase, and for getting in a decrease, in synaptic con ductance.     

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.     

Electroconvulsive shock effects on a reactivated memory trace: further examination

Rats showed amnesia for conditioned fear training if given an electroconvulsive shock immediately after training. Retention was unimpaired, however, when the electroconvulsive shock treatment was given 1 day after training immediately after the presentation of the stimulus used in the fear conditioning training. These results support the view that electroconvulsive shock disrupts memory trace consolidation but does not disrupt a recently reactivated memory trace.     

Theta rhythm: a temporal correlate of memory storage processes in the rat

We examined the amount of theta rhythm (4 to 9 hertz) in cortical electroencephalograms of rats for 30 minutes after training in one-trial tasks. Some animals received electroconvulsive shock after training. The amount of theta in the electroencephalogram after training was positively correlated with the degree of subsequent retention of a footshock, whether animals had received electroconvulsive shock or not.     

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.     

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.     

Memory impairment after subcutaneous injection of acetoxycycloheximide

Subcutaneous injection of 240 micrograms of acetoxycycloheximide in mice rapidly produces marked inhibition of cerebral protein synthesis. Treated mice were trained to escape shock by choosing the lighted limb of a T-maze. When trained five or more minutes after injection, they had a normal capacity to learn. They remembered normally 3 hours after training, but 6 hours after training they had markedly impaired retention. Amnesia persisted thereafter. Injections immediately after training had a less marked but significant amnesic effect. These studies suggest that protein synthesis is not necessary for learning or for memory for 3 hours after training but that it is required for long-term memory. The protein synthesis which appears to be necessary for long-term e3memory occurs during training, or within minutes after training, or both.     

Recovery from retrograde amnesia: a learning process

Retrograde amnesia was produced in rats by electroconvulsive shock. Memory recovered if the animals were given repeated test trials. Memory did not recover if steps were taken to reduce the conditioning properties of the test trials; the manipulations included eliminating the response, altering the apparatus cues, or extinguishing conditioned "fear" by confining animals to the apparatus during the first test trial.     

低氧条件下的冲刺训练对运动员生理生化指标的影响*

目的：研究低氧条件下的冲刺训练对运动员身体内葡萄糖、胰岛素、游离脂肪酸以及乳酸应激条件下的影响。方法：所有运动员都分别参加三组不同实验条件的训练,并且每组训练相隔7天。三组不同训练条件分别为：常氧压的冲刺运动（N组）;中等缺氧的冲刺运动（M组）;高度缺氧的冲刺运动(H组)。每组冲刺运动都在功率自行车上进行,每组运动为4次为时30s的冲刺运动,阻力都为10档,并辅以教练口头激励,每次冲刺运动后恢复6min,并记录每次运动员产生的最高功率以及平均功率。两种不同的低氧条件由低氧面具提供。训练后,分别在运动前抽取血液1次,以及在4次运动完成后5min,30min,60min,120min各取一次,并检测各项指标。结果：1.常氧压组与两组低氧压组相比,血细胞中的葡萄糖含量没有明显的差异,但是,与没有进入运动开始前相比较,冲刺运动后的5min内葡萄糖含量上升显著。2.只有在冲刺运动完成后2h后,体内脂肪酸含量才显著上升,并且与常氧压组和中等低氧压组相比较,高度缺氧组的游离脂肪酸上升更为明显,且与这两组差异显著。3.与运动开始前相比,运动后5min、30min、60min内体内乳酸含量高,且具有显著差异。但在120min后差异消失。4.运动结束后5min时体内胰岛素含量较高,且与开始运动前和运动结束后其他三个时间段相比,具有显著差异。     

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.     

Luteinizing hormone-releasing factor potentiates lordosis behavior in hypophysectomized ovariectomized female rats

Subcutaneous injection of luteinizing hormone-releasing factor (LRF) in estrogen-primed hypophysectomized, ovariectomized female rats facilitates the appearance of the lordosis response. The LRF effect on lordosis was seen 90, 180, and 360 minutes after injection. This effect could help to synchronize the female's mating behavior with the ovulatory discharge of luteinizing hormone.