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At least 343 records · Page 19Linked to original sources
PubMed1989

The effects of ibotenic acid lesions of the nucleus accumbens on spatial learning and extinction in the rat.

Rats with ibotenic acid lesions of the nucleus accumbens (N. Acc) were studied in two spatial learning paradigms: a T-maze and a Morris water maze. Learning of a spatial discrimination task and its reversal in the T-maze were disrupted by the N. Acc lesions. As both original and reversal learning were impaired, there was no evidence of a specific lesion effect on reversal learning. The lesioned rats did not perseverate excessively in their choice of the previously reinforced arm. There was evidence of behavioural inflexibility during extinction when the lesioned rats failed to slow the pace at which they ran the maze in the absence of reward. Spontaneous alternation was not significantly affected by the lesion. Acquisition of the second spatial task, locating the hidden platform in the Morris water maze, was also impaired. The lesioned rats did eventually learn the task and successfully reached the platform with similar latencies and heading errors to controls. Thus, the N. Acc lesion impaired but did not abolish spatial learning in the T-maze and the water maze. The deficits observed in this study may reflect a role for the N. Acc in the reorganisation of behaviour in response to external change.

Animals↗
PubMedDate not supplied

[Reversal of signal significance of stimuli in the avoidance reflex].

The course of reversal learning in go -- no go avoidance reflex differentiation in both cats and dogs was analysed in terms of interrelations between drive and instrumental reflex activity. When signalling properties of the conditioned stimuli were reversed, marked changes in the drive state of experimental animals occurred. The increase of the fear drive influenced both the transfer of the instrumental response to the new positive conditioned stimulus and the extinction of the response to the previously positive stimulus. The quality of the conditioned stimuli and their reflexogenic strength exerted clear effects on the fear drive and on the course of reversal learning. Prefrontal lesions affected the drive state and the conditioned reflex activity of the animals during the reversal learning.

Animals↗
PubMed1997

MK-801 administration during ethanol withdrawal in neonatal rat pups attenuates ethanol-induced behavioral deficits.

Alcohol exposure during development can produce central nervous system dysfunction, resulting in a wide range of behavioral alterations. The various mechanisms by which alcohol causes these behavioral changes, however, remain unknown. One mechanism that has been suggested is NMDA receptor-mediated excitotoxic cell death produced by ethanol withdrawal. The present study examined whether MK-801, an antagonist of the NMDA receptor that has been shown to protect against NMDA receptor-mediated excitotoxicity, could block alcohol's adverse effects on behavior. Sprague-Dawley rat pups were exposed to alcohol (6.0 g/kg) in a binge-like manner on postnatal day 6 using an artificial rearing procedure. Subjects then received an injection of MK-801 (0.1 mg/kg) or vehicle during withdrawal, 21 hr after ethanol exposure. At postnatal day 40, all subjects were tested on a serial spatial discrimination reversal task. Ethanol-exposed subjects were impaired in both discrimination and reversal learning, and committed a significantly greater number of perseverative-type errors, compared with controls. MK-801 administration during ethanol withdrawal significantly attenuated ethanol-induced deficits in reversal learning and increases in perseverative-type errors, whereas MK-801 exposure by itself had no significant effect on performance. Thus, exposure to MK-801 during ethanol withdrawal partially protected against alcohol-related disruptions in spatial reversal learning. These results support the suggestion that NMDA receptor-mediated excitotoxicity may be one mechanism by which alcohol induces behavioral teratogenicity.

Alcohol Withdrawal Delirium↗
PubMed2005

Encoding changes in orbitofrontal cortex in reversal-impaired aged rats.

Previous work in rats and primates has shown that normal aging can be associated with a decline in cognitive flexibility mediated by prefrontal circuits. For example, aged rats are impaired in rapid reversal learning, which in young rats depends critically on the orbitofrontal cortex. To assess whether aging-related reversal impairments reflect orbitofrontal dysfunction, we identified aged rats with reversal learning deficits and then recorded single units as these rats, along with unimpaired aged cohorts and young control rats, learned and reversed a series of odor discrimination problems. We found that the flexibility of neural correlates in orbitofrontal cortex was markedly diminished in aged rats characterized as reversal-impaired in initial training. In particular, although many cue-selective neurons in young and aged-unimpaired rats reversed odor preference when the odor-outcome associations were reversed, cue-selective neurons in reversal-impaired aged rats did not. In addition, outcome-expectant neurons in aged-impaired rats failed to become active during cue sampling after learning. These altered features of neural encoding could provide a basis for cognitive inflexibility associated with normal aging.

Action Potentials↗
PubMed1995

The differences in learning abilities between spontaneously hypertensive (SHR) and Wistar normotensive rats are cue dependent.

We examined the performance of spontaneously hypertensive (SHR) and Wistar normotensive (NT) rats in acquisition, retention after a 2-month interval, and reversal learning in two tasks: simultaneous brightness discrimination (Experiment I) and conditional discrimination of directional locomotor responses (Experiment II). In both tasks food reinforcement was used. In Experiment I both SHR and NT groups comprised younger (3-month-old) and older (10-month-old) rats. In each experimental stage SHRs of both age groups mastered the task earlier and made fewer errors than the respective NT groups. Reversal learning took longer than acquisition of discrimination in both age groups of NT rats. Conversely, reversal learning was an easier task for SHR. In Experiment II only younger rats were used. The forced turn at the start in the modified T-maze was utilized as the cue to guide performance at the choice point of the maze. In acquisition and retention, rats were trained to select at the choice point the arm in the same direction as in the forced turn; in the reversal, opposite contingencies were applied. At all stages the choice accuracy of SHR was the same as that in NT rats. The contrasting findings of Experiment I and Experiment II indicate that SHR learned better than NT when exteroceptive visual stimuli were used, but performed at the same level as NT rats in the task where interoceptive kinesthetic cues were relevant. We suggest that SHR pay more attention to visual stimuli than NT rats.

Age Factors↗
PubMed2001

Delivery across the blood-brain barrier of antisense directed against amyloid beta: reversal of learning and memory deficits in mice overexpressing amyloid precursor protein.

Amyloid beta protein (Abeta) may play a causal role in Alzheimer's disease. Previous work has shown that the learning and memory deficits that develop with aging in SAMP8 mice, a strain that overproduces Abeta, can be reversed with i.c.v. injections of an Abeta antisense phosphorothiolate oligonucleotide (Olg). Here, we showed that Olg radioactively labeled with (32)P (P-Olg) was transported intact across the blood-brain barrier (BBB) of mice by a saturable system, termed oligonucleotide transport system-1 (OTS-1). Multiple-time regression analysis found a blood-to-brain unidirectional influx rate for P-Olg of 1.4 +/- 0.39 microl/g-min and capillary depletion showed that P-Olg completely crossed the BBB to enter the parenchymal space of the brain. P-Olg was also shown to enter the cerebrospinal fluid. Transport was especially high into the hippocampus, with the percentage of the i.v. dose taken up by each gram of brain (0.865 +/- 0.115%) being about 1/100 of the i.c.v. dose. An i.v. dose of Olg 100 times that of the effective i.c.v. dose reversed the learning and memory deficits of aged SAMP8 mice. These studies show for the first time that phosphorothiolate oligonucleotides can be delivered to the brain in effective doses by intravenous administration.

Alzheimer Disease↗
PubMed1993

Crick and Mitchison's theory of REM sleep and neural networks.

Crick and Mitchison proposed that a reverse learning mechanism in REM sleep removes certain undesirable modes of interaction in neural networks within the cerebral cortex. If their theory is correct then abnormalities of reverse learning might account for some aspects of schizophrenia, mania, and depression. The theory of reverse learning might lead to an understanding of why lithium salts terminate manic episodes.

Animals↗
PubMed1989

Classical conditioning in patients with severe memory problems.

Classical conditioning is one of the most fundamental forms of learning, and yet little is known regarding the effects of brain injury on conditioning processes in humans. Three patients with temporal lobe lesions and severe memory problems were therefore assessed in terms of eyeblink conditioning, extinction, discrimination and reversal learning, and in one patient electrodermal conditioning was also investigated. The acquisition of conditioned responses was seen to be intact, but the evidence regarding extinction was ambiguous. All of the patients were impaired in discrimination learning and also reversal learning.

Adult↗
PubMedDate not supplied

Retrieval induces hippocampal-dependent reconsolidation of spatial memory.

Nonreinforced retrieval can cause extinction and/or reconsolidation, two processes that affect subsequent retrieval in opposite ways. Using the Morris water maze task we show that, in the rat, repeated nonreinforced expression of spatial memory causes extinction, which is unaffected by inhibition of protein synthesis within the CA1 region of the dorsal hippocampus. However, if the number of nonreinforced retrieval trials is insufficient to induce long-lasting extinction, then a hippocampal protein synthesis-dependent reconsolidation process recovers the original memory. Inhibition of hippocampal protein synthesis after reversal learning sessions impairs retention of the reversed preference and blocks persistence of the original one, suggesting that reversal learning involves reconsolidation rather than extinction of the original memory. Our results suggest the existence of a hippocampal protein synthesis-dependent reconsolidation process that operates to recover or update retrieval-weakened memories from incomplete extinction.

Animals↗
PubMed1992

Reversal of learning and memory impairments following lesion of the nucleus basalis magnocellularis (NBM) by concurrent noradrenergic depletion using DSP4 in the rat.

In the following study the behavioural effects of simultaneous lesion of the nucleus basalis magnocellularis (NBM) using ibotenic acid and noradrenergic depletion following a single i.p. administration of DSP4 (50 mg/kg) were examined in the rat. NBM lesion induced a deficit in acquisition of a reinforced T-maze alternation task, a working memory adaptation of a spatial navigation task in a water maze and 24 h retention in a passive avoidance task compared to sham controls. No effect of the lesion on a reference memory version of spatial navigation in a water maze task was found. Animals that received a combination of NBM lesion and DSP4 treatment showed no impairment on any of the tasks that were impaired by NBM lesion alone. This indicates a reversal of the learning and memory deficits consequent to NBM lesion by simultaneous noradrenergic depletion. NBM lesion induced a significant reduction in choline-acetyltransferase activity in the frontal cortex, and DSP4 induced a significant decrease in noradrenaline concentration in occipital cortex and hippocampus, confirming the effects of these treatments. These results suggest an interaction between central noradrenergic and cholinergic systems in learning and memory processes.

Adrenergic Agents↗
PubMed1989

Learning about rules but not about reward is impaired following lesions of the cholinergic projection to the hippocampus.

Common marmosets with bilateral ibotenic acid-induced destruction of the neurones of the vertical limb of the diagonal band of Broca, which provide the major cholinergic input to the hippocampal formation, were impaired on the acquisition but not on the retention of a repeated-trial visuospatial discrimination learning task. They were also impaired on serial spatial reversal learning (but not on serial object reversal learning), on acquisition of a trial-independent successive concurrent discrimination using novel objects (but not on acquisition of a comparable discrimination in which two familiar objects had predictable reward value) and were unable to acquire a difficult conditional object discrimination. It is argued that the role of the hippocampus is in the acquisition but not the retention of ruled-based behaviour (which includes spatial responding) in contrast to the acquisition of discriminations based on stimulus-reward association formation.

Animals↗
PubMed1998

Monkeys with rhinal cortex damage or neurotoxic hippocampal lesions are impaired on spatial scene learning and object reversals.

Rhesus monkeys (Macaca mulatta) with lesions of the rhinal cortex or parahippocampal gyrus (made by aspiration) or hippocampus (made with ibotenic acid) and unoperated controls were tested on object discrimination and reversal, place discrimination and reversal, and spatial scene learning to determine the contribution of these temporal lobe structures to these forms of learning and memory. Rhinal cortex lesions produced a severe deficit in object reversal learning; hippocampal lesions produced a milder deficit. Monkeys with rhinal cortex removals and those with hippocampal lesions were equally impaired on spatial scene learning. None of the lesions impaired place discrimination or reversal. These results argue against the idea that the mnemonic contributions of the rhinal cortex and hippocampus are limited to object and spatial domains, respectively.

Animals↗
PubMed2003

Acetylcholine actions in the dorsomedial striatum support the flexible shifting of response patterns.

There is accumulating evidence that the dorsomedial striatum plays a significant role in the learning of a new response pattern and the inhibiting of old response patterns when conditions demand a shift in strategies. This paper proposes that activity of cholinergic neurons in the dorsomedial striatum is critical for enabling behavioral flexibility when there is a change in task contingencies. Recent experimental findings are provided supporting this idea. Measuring acetylcholine efflux from the dorsomedial striatum during the acquisition and reversal learning of a spatial discrimination shows that acetylcholine efflux selectively increases during reversal learning as a rat begins to learn a newly reinforced spatial location, but returns to near basal levels when a rat reliably executes the new choice pattern. Experimental findings are also described indicating that the blockade of muscarinic cholinergic receptors in the dorsomedial striatum does not impair acquisition of an egocentric response discrimination, but impairs reversal learning of an egocentric response discrimination. Based on these results, increased cholinergic activity at muscarinic receptors is part of a neurochemical process in the dorsomedial striatum that allows inhibition of a previously relevant response pattern while learning a new response pattern. In situations that demand behavioral flexibility, muscarinic cholinergic activity in the dorsomedial striatum may directly influence corticostriatal plasticity to produce changes in response patterns.

Acetylcholine↗