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PubMed2001

Impairments in visual discrimination learning and recognition memory produced by neurotoxic lesions of rhinal cortex in rhesus monkeys.

Much work on the cognitive functions of the primate rhinal (i.e. entorhinal plus perirhinal) cortex has been based on aspiration lesions of this structure, which might disrupt fibres passing nearby and through the rhinal cortex in addition to removing the cell bodies of the rhinal cortex itself. To determine whether damage limited to the cell bodies of the rhinal cortex is sufficient to impair visual learning and memory, four rhesus monkeys (Macaca mulatta) were preoperatively trained on a battery of visual learning and memory tasks, including single-pair discrimination learning for primary reinforcement, single-pair discrimination reversals, concurrent discrimination learning and reversal, and delayed matching-to-sample. Following acquisition of these tasks and a preoperative performance test, ibotenic acid was injected bilaterally into the rhinal cortex, and the monkeys were retested. Consistent with the results of studies using aspiration lesions, the monkeys were impaired on single-pair discrimination learning as well as recognition memory performance postoperatively, although reliable reversal learning impairments were not observed. The magnitude of postoperative impairment in discrimination learning was not correlated with the magnitude of postoperative impairment in recognition memory, suggesting a possible dissociation between these functions within the rhinal cortex. The correspondence of behavioural deficits following aspiration and neurotoxic lesions of the rhinal cortex validates the attribution of various cognitive functions to this structure, based on the results of studies with aspiration lesions.

Animals↗
PubMed1989

Hemicholinium-3 impairs spatial learning and the deficit is reversed by cholinomimetics.

The effects of hemicholinium-3 (HC-3) on spatial discrimination learning were studied. Rats were equipped with indwelling cannulae in the right lateral ventricle and, following recovery, were trained on a two platform spatial discrimination task in a water maze. In this task a visible escape platform remains in a fixed position in the pool during a single training session, whilst the location of an identical "float" (which affords no escape) is randomly varied. For each session the location of the fixed escape platform was changed and the rats were retrained to criterion following pretreatment either with artificial cerebrospinal fluid (CSF) or HC-3 (2.5, 5.0 micrograms/rat/ICV) 1 h before training. Each rat received every treatment according to a latin square design. The results showed that spatial learning was dose dependently impaired by HC-3, choice accuracy being reduced to chance levels by the higher dose. There was no evidence of motoric difficulty, as choice latencies were not significantly increased. Experiments were then conducted to test for reversal of the deficit using a range of psychotropic drugs. Rats were treated with CSF or HC-3 (5 micrograms/rat ICV) 60 min prior to testing and test drugs were injected 15 min before testing. Some doses of physostigmine (46-460 micrograms/kg/SC) and tetrahydroaminoacridine (THA) (2.2-10 mg/kg/SC) reversed the spatial learning deficit. The muscarinic agonists arecoline (0.046-1 mg/kg/SC), aceclidine (1-10 mg/kg/SC), oxotremorine (30-100 micrograms/kg/SC) and RS-86 (0.46, 1.0 microgram/kg/SC) were also effective. Pilocarpine (0.22-2.2 mg/kg/SC) showed marginal activity and isoarecoline (4.6-10 mg/kg/SC) was inactive. Nicotine (0.32, 1, 3.2 mg/kg/SC) and piracetam (10, 30, 100 mg/kg IP) were also inactive. The alpha 2 agonist, clonidine (46, 100 micrograms/kg SC) and the antagonist idazoxan (32, 100 micrograms/kg SC) were also inactive. Learning deficits were not reversed by haloperidol (20, 60 micrograms/kg), amphetamine (0.1, 0.46 mg/kg), the selective 5-HT1A agonist 8-OH-DPAT (30, 100 micrograms/kg) or by the benzodiazapine antagonist ZK-93426 (1, 3.2, 10 mg/kg). The results show that forebrain Ach depletion by HC-3 impairs spatial discrimination learning and these deficits are reversed by cholinesterase inhibitors and some muscarinic receptor agonists. Some degree of pharmacological selectivity is indicated by the failure of a range of other drugs to reverse the impairments.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1981

Spatial discrimination, reversal and active or passive avoidance learning in rats with KA-induced neuronal depletions in dorsal hippocampus.

The neurotoxin kainic acid (KA) was iontophoretically administered to the dorsal hippocampus of female rats. Depending upon the diameter of the micropipette used to administered KA, this treatment completely depleted the dorsal hippocampus of nerve cell bodies (group LHC, N = 8) or selectively depleted CA4 (group SHC, N = 7) while sparing significant numbers of cells in CA1-CA3, and the fascia dentata. In both experimental groups, there was no apparent damage to the fimbria/fornix system, the ventral hippocampus and subiculum or neocortex adjacent to the injection site. The extensive neuron depletion (group LHC) sharply impaired the acquisition of a CAR in a shuttle box, produced a passive avoidance deficit in a step-through situation (but not in a punished-licking test), facilitated acquisition of a brightness discrimination in a T-maze, but had no significant effect on reversal learning in this situation. The more limited neuron depletions produced in group SHC produced no effect on CAR acquisition in the shuttle box but resulted in similar, though typically smaller effects in all other situations. The pronounced differences between this pattern of behavior change and that consistently reported after traditional lesions of the dorsal hippocampus indicate that damage to fibers of passage may contribute significantly to the classic hippocampal lesion syndrome.

Animals↗
PubMed1990

Effect of pyritinol, a cerebral protector, on learning and memory deficits induced by prenatal undernutrition and environmental impoverishment in young rats.

The study was conducted on 64 CF strain albino rats, which were equally distributed into 8 evenly matched groups following a 2 x 2 x 2 factorial design, by varying three independent factors at two levels: nutrition--normal and undernutrition; environment--enrichment and impoverishment, and drug treatment--vehicle and pyritinol (100 mg/kg, ip). Prenatal undernutrition was induced by restricting the mother's food intake. The environmental enrichment/impoverishment and the vehicle/pyritinol treatments were given during the postweaning period of the pups. The rats were subjected to original and subsequent reversal brightness discrimination learning tests in a single unit T-maze at 8-9 weeks of age. Thereafter, the animals were tested for the passive avoidance learning. The results indicate that undernutrition caused significant original discrimination learning deficits whereas environmental deprivation attenuated both the original and reversal learning performance. Environmental impoverishment attenuated the retention of passive avoidance behaviour but undernutrition had no effect on this paradigm. Pyritinol treatment improved the learning and retention performance of normally reared rats and also attenuated the original and reversal learning deficits induced by parental undernutrition and postweaning environmental impoverishment. The results indicate that pyritinol may be useful in learning and memory deficits induced by malnutrition and environmental deprivation.

Animals↗
PubMed1998

An attempt to distinguish between two reversal processing strategies for learning modeled motor skill.

The first purpose was to examine the effects of reversal processing strategy of visual information on recognition and acquisition of a sequential gross movement task. The second purpose was to examine the relationship between a measure of reversal processing strategy and movements during eye fixation. 24 undergraduates were assigned into one of three conditions, a Reversal-emphasized condition in which subjects were instructed to recognize the movement correctly from a reversed angle, a Recognition-emphasized condition in which subjects were instructed to recognize the movement correctly, and a Recall-emphasized condition in which subjects were instructed to reproduce the movement correctly. Subjects observed stimuli with the model facing them. Following observation, the subjects' recognition of stimuli was tested with model facing towards (Facing Angle) and facing away (Rear Angle). Recall tests were carried out after the two recognition tests. Analysis indicated that accuracy and response time on recognition tests improved under each condition, but there were no other effects. The Reversal-emphasized condition showed significantly greater modeling effect than the other conditions. Movements during eye fixation were very similar among conditions.

Adult↗
PubMed1996

Beta-amyloid accumulation correlates with cognitive dysfunction in the aged canine.

It is well known that beta-amyloid accumulates abnormally in Alzheimer's disease; however, beta-amyloid's relationship to cognitive dysfunction has not been clearly established and is often confounded by the presence of neurofibrillary tangles. We used canines to investigate the relationship between beta-amyloid accumulation and cognitive function in an animal model of aging lacking neurofibrillary tangles. The performance of 20 canines (11 purebred beagles and 9 mongrels) on a battery of six cognitive tasks was measured. These tasks included Reward Approach and Object Approach learning, as well as Discrimination, Reversal, Object Recognition, and Spatial learning and memory. Aged canines were impaired on some tasks but not others. beta-Amyloid-immunopositive plaques were found in many of the older animals. Plaques were all of the diffuse subtype and many contained intact neurons detected with double-labeling for neurofilaments. No neurofibrillary tangles were detected. beta-Amyloid was also associated with the processes of many neurons and with blood vessels. Using computerized image analysis, we quantified the area occupied by beta-amyloid in entorhinal cortex, frontal cortex, and cerebellum. Controlling for age-related increases in beta-amyloid, we observed that increased beta-amyloid deposition is strongly associated with deficits on Discrimination learning (r = .80), Reversal learning (r = .65), and Spatial learning (r = .54) but not the other tasks. There were a few differences between breeds which are discussed in the text. Overall, these data suggest that beta-amyloid deposition may be a contributing factor to age-related cognitive dysfunction prior to the onset of neurofibrillary tangle formation.

Alzheimer Disease↗
PubMed2000

The orbitofrontal cortex and reward.

The primate orbitofrontal cortex contains the secondary taste cortex, in which the reward value of taste is represented. It also contains the secondary and tertiary olfactory cortical areas, in which information about the identity and also about the reward value of odors is represented. The orbitofrontal cortex also receives information about the sight of objects and faces from the temporal lobe cortical visual areas, and neurons in it learn and reverse the visual stimulus to which they respond when the association of the visual stimulus with a primary reinforcing stimulus (such as a taste reward) is reversed. However, the orbitofrontal cortex is involved in representing negative reinforcers (punishers) too, such as aversive taste, and in rapid stimulus-reinforcement association learning for both positive and negative primary reinforcers. In complementary neuroimaging studies in humans it is being found that areas of the orbitofrontal cortex (and connected subgenual cingulate cortex) are activated by pleasant touch, by painful touch, by rewarding and aversive taste, and by odor. Damage to the orbitofrontal cortex in humans can impair the learning and reversal of stimulus- reinforcement associations, and thus the correction of behavioral responses when these are no longer appropriate because previous reinforcement contingencies change. This evidence thus shows that the orbitofrontal cortex is involved in decoding and representing some primary reinforcers such as taste and touch; in learning and reversing associations of visual and other stimuli to these primary reinforcers; and in controlling and correcting reward-related and punishment-related behavior, and thus in emotion.

Afferent Pathways↗
PubMed2007

Reversing the truth effect: learning the interpretation of processing fluency in judgments of truth.

Repeated statements receive higher truth ratings than new statements. Given that repetition leads to greater experienced processing fluency, the author proposes that fluency is used in truth judgments according to its ecological validity. Thus, the truth effect occurs because people learn that fluency and truth tend to be positively correlated. Three experiments tested this notion. Experiment 1 replicated the truth effect by directly manipulating processing fluency; Experiment 2 reversed the effect by manipulating the correlation between fluency and truth in a learning phase. Experiment 3 generalized this reversal by showing a transfer of a negative correlation between perceptual fluency (due to color contrast) and truth to truth judgments when fluency is due to prior exposure (i.e., repetition).

Cues↗
PubMed1982

Selective, naloxone-reversible morphine depression of learned behavioral and hippocampal responses.

Morphine administered intravenously causes immediate and complete abolition of a simple learned response (classically conditioned nictitating membrane extension in rabbit) and of the associated learning-induced increase in hippocampal neuron activity. Both effects are completely reversed by low doses of naloxone. Morphine has no effect at all on behavioral performance of the unconditioned reflex response.

Animals↗