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Biomedical subjects

W W Beatty

Publications and source records attributed to W W Beatty.

At least 73 records · Page 4Linked to original sources
PubMed1986

Further analysis of encoding in patients with Huntington's disease.

Arguments favoring the view that derangement of normal encoding processes contributes to the memory defects of patients with Huntington's disease (HD) are supported by the finding that HD patients do not learn highly imageable words more rapidly than they learn words that are difficult to image. But other data indicating that HD patients can use verbal mediators as mnemonic aids for picture recognition question the existence of important and general encoding deficits in HD. In the first of two experiments the influence of imagery on the acquisition and recall of 14-word lists was studied using a free-recall paradigm. Both HD patients and controls learned highly imageable words more quickly and retained them better than low imagery words over a 30-min delay. The impact of imagery on learning was apparent by the first trial. In the second experiment, a modified Brown-Peterson distractor paradigm was used to assess release from proactive interference (PI). It was found that both HD patients and controls exhibited comparable release from PI following a shift in taxonomic categories. The results of both experiments question the importance of encoding deficits in the memorial dysfunctions associated with HD.

Adult↗
PubMed1986

Patterns of memory failure after scopolamine treatment: implications for cholinergic hypotheses of dementia.

To test the idea that scopolamine provides a suitable pharmacological model of the memory defects associated with cortical or subcortical dementias, we assessed memory on a battery of tasks in healthy young normal subjects who received 0.5 mg scopolamine, 0.1-0.2 mg glycopyrrolate or physiological saline, once each on three separate occasions, and compared the pattern of memory failure induced by scopolamine to that observed on the same tasks in patients with Alzheimer's disease (AD) or Huntington's disease (HD). In agreement with previous reports, scopolamine impaired acquisition and delayed recall of a 14-word list and disrupted retention on the Brown-Peterson distractor task, whereas the peripherally active anticholinergic glycopyrrolate was without effect. However, under scopolamine the pattern of errors made on these memory tasks was quite different from that seen in patients with AD. Scopolamine did not increase the number of false positive errors on delayed recognition of the word list and also failed to increase the number of prior-item intrusions on the Brown-Peterson task. Also, scopolamine did not impair learning of a symbol-digit paired-associate task, and did not reduce the number of words retrieved or increase the number of words repeated on a standardized verbal fluency test. When the effects of scopolamine on memory were compared to the pattern of impairments observed in demented patients with HD, several differences were found. Although scopolamine clearly produces deficits on some measures of anterograde memory, the present findings question whether anticholinergic drugs adequately mimic the full range of memory impairments observed in cortical or subcortical dementias.

Adult↗
PubMed1986

Preserved spatial memory in old rats survives 10 months without training.

Aged rats with extensive prior training on the radial maze retain the capacity for accurate spatial working memory (WM) for at least 3 months without practice. To investigate the temporal limits of this influence of prior experience we compared the reacquisition of spatial WM by a group of experienced 21.5-month-old rats to the original acquisition by naive 3-month-old rats. The aged rats had received 225 radial maze tests between 3 and 11 months of age. Despite 10 months without practice the old rats rapidly reacquired critical performance. Their reacquisition was markedly superior to original learning by the young rats, even when delays as long as 5 h were imposed between the rats' fourth and fifth choices during the daily tests in the eight-arm maze. Additional tests showed that neither young nor old rats employed a response strategy to maintain accurate spatial WM performance. Experience clearly confers long-lived protection against the otherwise deleterious effects of aging on spatial WM, but the mechanism by which this influence arises is unknown.

Aging↗
PubMed1985

Spatial memory of children and adults assessed in the radial maze.

To assess the development of accurate spatial memory and its relationship to organized search strategies, children (18-71 months old) and college students searched for rewards hidden at the ends of the arms of an eight-arm radial maze. Subjects made their first four choices in random order selected by the experimenter (forced choice) or in whatever order they wished (free choice). In some conditions, a retention interval was imposed between arm choices 4 and 5, followed by a resumption of the task. With free choice, accuracy of spatial memory increased linearly with age, and the proportion of tests on which the child entered four adjacent arms in sequence during the first four choices, a measure of organized searching, also increased linearly with age. Disrupting this sequential search strategy (forced choice) reduced accuracy for both children and college students, although the reduction with college students was small. Delays had minimal effects for children who met criterion at 0-delay and for college students. Although response patterns seem unimportant in accurate spatial memory in rats, systematic search strategies mature together with, and probably contribute to, the improvement of spatial memory with age in humans.

Adolescent↗
PubMed1985

Scopolamine degrades spatial working memory but spares spatial reference memory: dissimilarity of anticholinergic effect and restriction of distal visual cues.

The influence of the centrally active anticholinergic, scopolamine hydrobromide, on working and reference memory was studied in rats tested in a 12-arm radial maze. Both 0.25 and 0.5 mg/kg doses of the drug increased the number of working memory (WM) errors but had no effect on reference memory (RM) errors. A lower dose (0.125 mg/kg) was ineffective, as was the peripherally active anticholinergic, scopolamine methylbromide (0.5 mg/kg). Some of the behavioral effects of anticholinergics on spatial memory are mimicked by blindness or eliminating distal visual cues. If distal visual cues were more important for maintaining accurate WM than for RM, the selective effect of scopolamine on WM could be easily explained. But surrounding the maze with a curtain to eliminate extramaze cues increased RM errors without significantly increasing WM errors. Thus, the selective effect of anticholinergies on spatial memory in the radial maze is qualitatively different from the effect of restricting distal visual cues and must arise from some other action of the drug.

Animals↗
PubMed1985

Preservation of accurate spatial memory in aged rats.

Male rats were tested in an 8 arm radial maze from 6-26 months of age with 5 hr delay imposed between choices 4 and 5. At 26 months their spatial memory was more accurate than when they were first tested at 6 months and also more accurate than that exhibited by another 5 month old group tested concurrently. However, these old rats acquired a noval spatial habit more slowly than the younger animals. In a subsequent study, we compared the acquisition of accurate spatial memory by rats that were 3 or 21.5 months old at the start of training. Older rats adapted to the maze more slowly and required more sessions to achieve criterion with no delay imposed during the test. There was no reliable difference in acquisition when a 1 hr delay was imposed between choices 4 and 5, but the old rats learned more slowly with a 5 hr delay. On memory tests after criterion performance had been achieved, the older rats performed as well as the younger animals at all delay intervals. Aged rats are deficient in acquiring the skills required for accurate spatial memory, but once acquired these skills do not deteriorate. The possibility that other "memory" deficits associated with aging might be alleviated by overtraining is discussed.

Adaptation, Psychological↗
PubMed1985

Spatial memory in rats: electroconvulsive shock selectively disrupts working memory but spares reference memory.

In two experiments rats were trained until they displayed highly accurate spatial memories when a 4-h delay was imposed between the to-be-remembered event (TBRE) and the retention test in a 12-arm radial maze. If the procedure tested only working memory (WM) electronvulsive shock (ECS) 2 h after the TBRE produced amnesia but ECS immediately after the TBRE was ineffective. If the testing procedure also involved a reference memory (RM) component, ECS degraded WM regardless of whether it was given 0 or 2 h after the TBRE. RM was not affected. With either training procedure administering ECS 2 h before the TBRE was ineffective. Thus, in the radial maze truly old spatial RM was immune to disruption by ECS while more recent WM was vulnerable. Possible explanations of the data are presented.

Animals↗
PubMed1985

Sensory and social influences on ice cream consumption by males and females in a laboratory setting.

Both male and female undergraduates ate more ice cream when eating occurred in groups of three or four than when they ate alone. These subjects also ate more ice cream when offered three different flavors than when offered only one flavor of their own choosing. For women, both variety and eating in a group combined to enhance eating more than either variable did alone. For men, variety or eating in a group caused about the same enhancement of consumption but the combination of the two variables did not lead to further increases in intake. This latter result probably reflects a ceiling effect, but it could represent a true gender difference.

Adult↗
PubMed1985

Antidepressant treatment of children: clinical relapse is unrelated to tricyclic plasma concentrations.

Plasma concentrations of imipramine and amitriptyline and their desmethylated metabolites were measured in 20 children being treated for major depressive illness 2 wk. and 5 to 10 wk. after achieving drug dosages of 2.25 mg/kg body weight. At 2 wk. all children had exhibited clinical improvement, but by 10 wk. 4 of the 10 children treated with imipramine and 5 of the 10 children treated with amitriptyline had experienced clinical relapse of depressive symptoms. Tricyclic antidepressant plasma concentrations and ratios were comparable in the subgroups of children who maintained their clinical improvement and those who relapsed. There was no evidence of a systematic decline in plasma tricyclic antidepressant concentrations in those children who relapsed.

Adolescent↗
PubMed1984

Suppression of play fighting by amphetamine: effects of catecholamine antagonists, agonists and synthesis inhibitors.

Moderate doses of amphetamine and methylphenidate profoundly depress play fighting in juvenile rats. To test the idea that this behavioral effect was dependent on the release of catecholamines (CAs) we administered haloperidol (0.05-0.8 mg/kg), chlorpromazine (0.5-5 mg/kg), phenoxybenzamine (0.5-20 mg/kg) or propranolol (0.5-20 mg/kg) alone or in combination with 0.5 or 1 mg/kg d-amphetamine sulfate. None of these CA antagonists reversed the suppression of play fighting (indexed by pinning) caused by amphetamine, but at higher doses haloperidol, chlorpromazine and phenoxybenzamine depressed both pinning and rearing. The presynaptic NE agonist clonidine (0.05-0.2 mg/kg) also failed to block the effects of amphetamine on play; instead it too depressed both pinning and rearing. Finally the CA synthesis inhibitor, alpha-methyltyrosine (total dose: 100 mg/kg) did not attenuate the suppression of play by amphetamine. Ephedrine (10-80 mg/kg) mimicked the effects of amphetamine on pinning, but apomorphine did not. At doses from 0.125-0.5 mg/kg apomorphine stimulated pinning while 1 mg/kg had no effect. The present findings confirm earlier reports that amphetamine suppresses play fighting but the mechanism of action remains obscure.

Aggression↗
PubMed1984

Spatial memory over long retention intervals: nonmemorial factors are not necessary for accurate performance on the radial-arm maze by rats.

A. Markowska, O. Buresová, and J. Bures (1983, Behavioral and Neural Biology, 38, 97-112) argued that the apparent persistence of accurate spatial working memory over delays of several hours arises from the formation of response strategies and the use of olfactory stimuli that develop with extended training at long delays. To test this explanation rats with extensive prior training at long delays were forced to enter the first four arms in a random order. On test days, the maze was rotated 180 degrees during the 2-h retention interval to determine whether the rats were using intramaze or extramaze (i.e., spatial) cues to guide their choices. On both rotation and control days, postdelay choices were spatially guided, averaging over 90% correct. Accurate spatial working memory at long delays is a reproducible phenomenon and does not appear to result from nonmemorial artifacts.

Animals↗
PubMed1984

Amphetamine disrupts both working and reference memories of rats trained in a radial maze.

To assess the effects of amphetamine on working and reference memory rats were trained on a 12-arm radial maze with six arms baited and six arms unbaited until stable performance was achieved. Administration of 2.0 mg/kg d-amphetamine sulfate increased both working and reference memory errors, but only if a 5-min delay was imposed after three successful choices. With no delay this dose had no reliable effect on either working or reference memory. Lower doses (0.5 or 1.0 mg/kg) were ineffective even when a delay was imposed during the test. We suggest that amphetamine heightens arousal, which disrupts accurate retention when the rat's attention to the relevant cues is interrupted, as during a brief delay. Alternative explanations are discussed.

Animals↗
PubMed1983

Medial hypothalamic lesions and play fighting in juvenile rats.

The effects of medial preoptic area (MPOA), anterior hypothalamic (AH) and ventromedial hypothalamic (VMH) lesions on play fighting were studied in juvenile rats that were housed and observed in heterosexual groups of 6-8 animals. Overall males engaged in play fighting more frequently than females and none of the lesions reliably affected this measure. Males also initiated more play fights. AH and VMH lesions reduced the frequency of play initiation in both sexes, but MPOA lesions had no reliable effect in either sex.

Age Factors↗
PubMed1983

Olfactory bulbectomy and play fighting in juvenile rats.

To determine the influence on play fighting of inputs to the brain that arise in or course through the olfactory bulbs juvenile male and female rats were bilaterally bulbectomized at 23 or 24 days of age. The frequency of play fighting and play initiation was observed in tests conducted in the home cage. Bulbectomy did not affect the frequency of play fighting or play initiation by males, but slightly increased the frequency of play fighting without altering play initiation in females. Since peripheral anosmia has only modest effects on play fighting, neither the chemosensory nor the modulatory influences of the olfactory bulbs on limbic system activity appear to be especially important in the control of play by juvenile rats.

Aggression↗
PubMed1983

Opiate antagonists, morphine and spatial memory in rats.

To assess the possible role of endogenous opioids on spatial memory, rats were administered morphine (1-15 mg/kg), naloxone (1-10 mg/kg), or naltrexone (0.1-10 mg/kg) at varying times after or prior to completing the first 4 choices in an 8 arm radial maze. None of these agents consistently affected retention, suggesting that endogenous opioid systems do not play a major role in modulating neural mechanisms that maintain accurate spatial memory.

Animals↗
PubMed1983

Spatial working memory in rats: effects of monoaminergic antagonists.

To assess the possible involvement of the monoaminergic neurotransmitters norepinephrine, dopamine and serotonin in the maintenance of spatial working memory rats were treated with antagonists 0 or 2 hr after completing the first 4 choices in an 8 arm maze. Haloperidol (0.25-1 mg/kg), when administered 2 hr after Choice 4, produced a small but consistent impairment in performance on retention tests given 5 hr after the first 4 choices. This deficit closely resembled natural forgetting in terms of the type of errors committed. By contrast, haloperidol in the same doses given 0 hr after Choice 4 or 3 hr before the first 4 choices did not affect retention. Likewise treatment with propranolol (10-20 mg/kg), phentolamine (5-20 mg/kg) or methysergide (5-15 mg/kg) did not impair spatial memory, regardless of when these drugs were injected within the session. Evidently dopaminergic neuronal systems are important in the maintenance of normal spatial working memory.

Animals↗
PubMed1983

Retention deficit after d-amphetamine treatment: memory defect or performance change?

Retention deficits in discrete trial delayed alternation and delayed matching to sample tasks following administration of d-amphetamine have been interpreted to support the view that arousal facilitates the decay of information from shortterm memory (STM) (Kesner, 1973). But since amphetamine causes numerous changes in performance, alternative explanations of the deficit are also plausible. In an attempt to separate drug effects on memory from those on performance, the effects of d-amphetamine on spatial memory in the radial maze were studied in rats. The unusually long span of accurate working memory in this setting permits drug administration within the retention interval as well as prior to the to-be-remembered event (TBRE). In rats tested at a 5-hr retention interval d-amphetamine (2 mg/kg) disrupted retention when given 0.5 hr before or 4.5 hr after the TBRE, but the same treatment 0 or 2 hr after the TBRE or 3 hr before the TBRE was without effect. At a 5-hr retention interval 3 mg/kg d-amphetamine impaired performance if given 2 hr after the TBRE, but not when given 0 hr after the TBRE or 3 hr before the TBRE. However, when the retention interval was lengthened to 7 hr, administering 3 mg/kg d-amphetamine 2 hr after the TBRE did not disrupt performance. The effects of d-amphetamine on spatial memory are best explained in terms of the well established effects of the drug on motor activity and appetite. Similar changes in performance may account for the "memory" impairments observed after amphetamine treatment in other tasks.

Animals↗