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Query: UMLS:C0598853 (forgetting)
3,232 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were trained on a continuously reinforced bar-press response for water reward. Seven days later they were retested for retention, with or without pretest injection of the nootropic drug, piracetam. Drug-treated animals had significantly shorter response latencies than saline-treated animals. The results are interpreted as a facilitation of retrieval processes after forgetting. The experiment was extended under extinction conditions and it was found that after three sessions there was a tendency to facilitate extinction when response latency is used as the extinction index. The clinical interest of a drug which facilitates the retrieval aspect of the memory process without impairing extinction is discussed.
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PMID:Piracetam facilitates retrieval but does not impair extinction of bar-pressing in rats. 10 22

Benzodiazepine and anticholinergic drugs interfere with septo-hippocampal function in similar but not identical ways. They also share a number of common behavioural effects and, in particular, both classes of drug interfere with spatial memory in the Morris Water Maze--a test which is very sensitive to hippocampal dysfunction. We have previously shown that the anticholinergic drug scopolamine impairs discriminability, but not rate of forgetting, in delayed conditional discrimination. In the present study forgetting was quantified by fitting a negative exponential function to estimates of discriminability derived from a signal detection analysis of data from an auditory delayed conditional discrimination task. Chlordiazepoxide produced a highly significant decrease in discriminability which was monotonically related to the logarithm of dose in the range 0.67-18.0 mg/kg IP. The rate of forgetting was not increased. These data confirm the pharmacological independence of changes in discriminability and rate of forgetting; demonstrate that in this task chlordiazepoxide has similar effects to scopolamine; and suggest that the effects of chlordiazepoxide in other working memory tasks could be more a result of changed stimulus processing than impairment of memorial processes.
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PMID:Chlordiazepoxide reduces discriminability but not rate of forgetting in delayed conditional discrimination. 238 77

Interactions between the neuromodulators acetylcholine and norepinephrine (NE) have been reported in both developmental neural plasticity and learning and memory. In a test of the generality of this phenomenon, we assessed the amnestic effects of the muscarinic antagonist scopolamine in normal and NE-depleted mice. Pretraining administration of scopolamine impaired 24-h retention of inhibitory (passive) avoidance training (at doses of 0.1, 0.3 and 1.0 mg/kg) and the acquisition of place-training in a water maze (at a dose of 1.0 mg/kg). NE depletion resulting from systemic administration of DSP-4 did not affect performance on these tasks and did not significantly alter the effects of scopolamine. NE depletion did, however, impair the retention of place learning when mice were retested 16 days after initial training; and this impairment in the retest was additive with one observed in mice originally trained under scopolamine. Normal acquisition but rapid forgetting has also been reported in aged rodents, who display deterioration of the noradrenergic system. Thus, observation of a similar pattern of performance consequent to experimental NE depletion suggests a role for noradrenergic dysfunction in age-related memory decline.
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PMID:Effects of concurrent manipulations of cholinergic and noradrenergic function on learning and retention in mice. 270 90

Rats were given continuous intraventricular infusion of saline or the thiol-proteinase inhibitor leupeptin, via subcutaneously implanted osmotic minipumps, while being trained on a spatial learning water task using spaced trials. Leupeptin caused overnight forgetting during training, but performance eventually reached asymptote in both groups. A retention test conducted 48 h later to assess spatial memory revealed no significant group differences, but did cause, in saline-treated rats only, a disruption of subsequent retraining back to the correct spatial location. The groups showed no differences in Cl-dependent [3H]glutamate receptor binding to hippocampal or entorhinal cortex membranes subsequent to training. In a second experiment, normal rats trained on the same task also showed no differences in Cl-dependent [3H]glutamate binding relative to rats exposed to the water task but given random spatial position training and handled controls. The results are discussed in relation to the hypothesis of Lynch and Baudry (Science (1984) 224, 1057-1063) that a calcium-dependent thiol proteinase is involved in memory formation through its ability to modify glutamate receptor distribution and dendritic spine shape.
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PMID:Spatial learning in the rat: impairment induced by the thiol-proteinase inhibitor, leupeptin, and an analysis of [3H]glutamate receptor binding in relation to learning. 288 15

The generality of amphetamine-induced retrieval enhancement was investigated by determining whether pretest administration could alleviate different types of forgetting. Thirsty mice were punished for licking a water tube following a period of free drinking. Forgetting of the conditioned drink suppression was induced in different groups of animals by; protein synthesis inhibition, cholinergic receptor blockade, inhibition of norepinephrine synthesis, stimulation of serotonin receptors, electroconvulsive shock, a 2.5 month training to test interval and the use of senescent animals with an endogenous memory defect. Thirty min prior to testing mice were injected with either saline or with 2 mg/kg d-amphetamine sulphate. Results showed that amphetamine produced a highly significant improvement in remembering in all of the forgetting treatment groups. It is concluded that amphetamine can alleviate forgetting caused by widely diverse etiologies probably by activating a nonspecific general retrieval system.
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PMID:Amphetamine enhances retrieval following diverse sources of forgetting. 321 62

Male mice of the BALB/c strain were given a solution of 12% v/v ethanol as their only source of fluid for 7 months. Memory performance was tested after ethanol was omitted from the diet for 3 to 9 weeks, and was compared with performance of control animals (no ethanol) which had been pair-fed or had received tap water. The spontaneous alternation task that was used consisted of two forced trials (acquisition) followed, at varying intervals ranging from 30 sec to 6 hr, by a free test trial (retention). Experimental subjects exhibited an accelerated rate of decay of spontaneous alternation, reaching chance level at 6 hours. All animals were then tested at this 6-hour interval following injections of either physostigmine or neostigmine that were given before both acquisition and retention (0.05 mg/kg IP). Results showed that physostigmine, but not neostigmine, dramatically improved performance of alcohol-treated subjects. Parallel neurochemical analysis showed that chronic ethanol treatment induced a slight (12%) but significant decrease in hippocampal sodium-dependent high affinity choline uptake. Though these findings suggest that the observed memory deficits (i.e., an accelerated rate of forgetting) might be related to a cholinergic dysfunction, alternative explanations are also proposed.
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PMID:On the involvement of the central cholinergic system in memory deficits induced by long term ethanol consumption in mice. 370 88

Male mice of the BALB/c strain were given a solution of 15% ethanol as their only source of fluid for periods varying from 5 weeks to 8 months. For behavioral testing, they were compared with control groups which had received either an isocaloric solution of sucrose or tap water. Memory was tested by using spontaneous alternation behavior in a T maze. Each test consisted of two forced trials (acquisition) followed by a free trial (test) given at different acquisition--test intervals (from 30 s to 24 h). Results from two independent experiments showed that after 25 weeks of ethanol administration there was an accelerated rate of decay of spontaneous alternation as a function of the acquisition--test interval. Such a phenomenon persisted after ethanol was omitted from the diet. A third experiment showed that when tested on two successive sessions separated by a 5 h interval, experimental subjects exhibited a decreased ability to perform normally on the second test. Our data are interpreted as showing that long-term ethanol administration results in accelerated forgetting and increased vulnerability to proactive interference and, as such, they are compared to the memory dysfunctions observed in amnesic patients.
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PMID:Memory deficits subsequent to chronic consumption of alcohol in mice: an analysis based on spontaneous alternation behavior. 397 84

Male Mice of the BALB/c strain were given a solution of 15% ethanol as its only source of fluid for 8 months. 2 months after alcohols was omitted from the diet they were tested for memory and compared to two control groups which received either an isocaloric solution of sucrose or tap water. Memory was tested by using spontaneous alternation (S.A.) in a T maze as a learning paradigm involving two forced trials (acquisition) followed by a free trial (retention). The 1st experiment was aimed at studying the spontaneous alteration rate as a function of the acquisition-test interval. It was found that for a short interval (5 min) the S.A. rate did not differ between the experimental aid control subjects but that it decreases more rapidly over time (1 h and 24 h) in alcohol treated subjects. The second experiment was aimed at determining whether this accelerated forgetting might not be explained by an excess of proactive interference. Results showed that when experimental subjects remembered for 1 h informations associated with a first acquisition, they were no longer able to remember those associated with a second acquisition when the interval between the two acquisitions was 5 h. Such proactive interference was not found in control subjects. These results suggest that, as in humans, prolonged alcohol consumption results in accelerated forgetting and increased proactive interferences.
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PMID:[Accelerated forgetting and increased proactive interference after long-term alcohol consumption in the mouse]. 640 62

Rats were trained on a succession of two-odor discriminations for a water reward in a modified radial maze. A different odor pair was used each day. After three or four pairs, rats would learn to choose the correct odor in only 3-5 trials. Animals were then subjected to electrolytic lesions in the lateral entorhinal cortex, which is innervated by the lateral olfactory tract, or in the dorsal entorhinal cortex, which is not a target of the olfactory system. Lesions of the first type did not interfere with performance, provided a short interval (30 sec to 2 min) was used between trials. However, the rats were severely impaired when trials were separated by 3-10 min. Dorsal lesions had no effect on olfactory discrimination irrespective of length of delay. In additional experiments, the rats were trained for 10 trials with short inter-trial intervals and then tested 1 hr later with the significance of the cues reversed. Animals with dorsal lesions continued to respond to the formerly correct odor while those with lateral entorhinal damage immediately reversed their response choices. These results provide evidence that lesions to the hippocampal system produce a rapid forgetting syndrome in rats comparable with that reported for humans with temporal lobe damage or dysfunction.
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PMID:Hippocampal denervation causes rapid forgetting of olfactory information in rats. 659 92

This study determined whether prior habituation to water immersion would ameliorate age-related deficits in learning and memory in a swim task. Aged (22 months) and young adult (3 months) rats were immersed in water (30 degrees C) for 15 min on each of 28 consecutive days before training in the swim task. Additional groups of age-matched animals served as handled controls. Training on a spatial discrimination version of the water task was conducted over 5 days with two trials per day (1-h intertrial interval). A probe trial was substituted for the last trial on the fifth day to assess the rats' use of spatial information. Three days later, rats received cue discrimination training to find a visible platform. In the spatial task, prior habituation to water immersion ameliorated deficits in acquisition within each day (i.e., at a 1-h intertrial interval) but not across days (at 24 h). The results obtained with the 24-h interval confirm the rapid forgetting characteristic of aged rats in many tasks. The stress-habituation procedures reduced age-related deficits seen on the probe trial and on cue discrimination training. These findings indicate that several aspects of age-related impairments in the swim task, often attributed to primary age-related deficits in learning and memory processes per se, may instead be secondary to age-related differences in stress responses to water immersion.
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PMID:Age and stress history effects on spatial performance in a swim task in Fischer-344 rats. 866 Dec 46


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