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Biomedical subjects

N M White

Publications and source records attributed to N M White.

At least 55 records · Page 3Linked to original sources
PubMed1990

6-Hydroxydopamine lesions of the olfactory tubercle do not alter (+)-amphetamine-conditioned place preference.

Rats received bilateral infusions of 6-hydroxydopamine into the olfactory tubercle, resulting in a substantial (89%) local depletion of dopamine. This treatment did not significantly alter conditioned place preference produced by (+)-amphetamine, suggesting that the mesolimbic dopaminergic projection to olfactory tubercle does not mediate the rewarding effects of (+)-amphetamine in rats.

Amphetamine↗
PubMed1990

Lesions of the caudate nucleus selectively impair "reference memory" acquisition in the radial maze.

Groups of Long-Evans rats with bilateral lesions of the caudate nucleus, sham lesions, or no lesions were given one trial per day in an eight-arm radial maze. The same four maze arms were baited on each trial. The remaining four arms never contained food. Optimal performance required animals to enter each of the baited arms only once on each trial and to avoid entering the arms in the unbaited set. Rats with caudate lesions learned to enter each of the baited arms only once on each trial. However, these rats were severely impaired in learning to avoid entering the arms in the unbaited set. Implications for dual-memory theories are discussed.

Animals↗
PubMed1990

Acute myocardial infarction resulting from the migration of a Greenfield filter.

A paraplegic patient who underwent the placement of Greenfield filters to prevent pulmonary emboli had one of the filters migrate proximally to the junction of the inferior vena cava and right atrium, then into the right atrium a few months later. This resulted in an acute myocardial infarction by apparently causing an intimal dissection of the posterior descending artery. Treatment, follow-up and causes of filter migration are discussed.

Adult↗
PubMed1989

Effectiveness of two methods of parenteral nutrition support in improving muscle mass of children with neuroblastoma or Wilms' tumor. A randomized study.

The short-term and long-term effectiveness of central parenteral nutrition (CPN) versus peripheral parenteral nutrition (PPN) in improving muscle mass (arm muscle area [AMA]) was evaluated for 24 malnourished children with newly diagnosed Stage IV neuroblastoma (n = 14) or Stages II-V Wilms' tumor (n = 10). Patients were randomized to either CPN or PPN plus enteral nutrition (EN: intense nutrition counseling, oral foods, and supplements) for 4 weeks followed by EN until week 10. Oncologic treatment was similar for each tumor type. Dietary, anthropometric, and biochemical measurements were obtained at weeks 0, 4, and 10. During weeks 1 through 4, energy (CPN: means 100 +/- 4; PPN: means 96 +/- 4% of healthy children) and protein (CPN: means 2.5 +/- 0.1; PPN means 2.7 +/- 0.2 g/kg) intakes of the two groups did not differ. The AMA increased (P less than 0.05) with 4 weeks of CPN but not with PPN; changes thereafter with EN were not significant. Weight (P less than 0.05) and triceps skinfolds (P less than 0.01) increased with 4 weeks of PN in both groups and decreased with EN thereafter (P less than 0.01) but were higher at week 10 than diagnosis. Increases in albumin in both groups reached significance at week 10 (P less than 0.05). These data show that CPN improves AMA in malnourished children with neuroblastoma or Wilms' tumor when energy and protein intakes are adequate. The AMA gains can be maintained thereafter with EN.

Anthropometry↗
PubMed1989

Dissociation of visual and olfactory conditioning in the neostriatum of rats.

In an experiment designed to demonstrate a double dissociation, the effects of bilateral electrolytic lesions of either the posteroventral or the ventrolateral regions of the neostriatum on the conditioned emotional response (CER) were examined. Posteroventral lesions impaired acquisition of the CER with a visual CS but not with an olfactory CS. Sham-operated posteroventral and ventrolateral lesioned animals acquired the visual CER normally. Ventrolateral lesions impaired acquisition of the CER with the olfactory CS but not with the visual CS. Sham-operated ventrolateral and posteroventral lesioned animals acquired the olfactory CER normally. In a second experiment the effect of post-training unilateral intrastriatal microinjections of (+)-amphetamine on acquisition of the visual and olfactory CERs was studied. Posteroventral injections improved retention of the visual, but not the olfactory CER. Ventrolateral injections improved retention of the olfactory, but not the visual CER. Saline and delayed (+)-amphetamine injection controls demonstrated that the improvement of retention in each case was a retroactive improvement of memory for the recently acquired CERs by (+)-amphetamine. These findings are consistent with previous reports of post-training memory facilitation mediated by dopaminergic function in the neostriatum. The results of both experiments are consistent with a regional functional heterogeneity hypothesis: the idea that anatomically linked areas of cortex and neostriatum process memories involving different stimuli in similar ways and that the integrity of these structures and their connections is necessary to establish and consolidate associative memory.

Amphetamine↗
PubMed1989

A functional hypothesis concerning the striatal matrix and patches: mediation of S-R memory and reward.

Recent neurochemical and anatomical findings delineating two compartments, the patches and the matrix, in the mammalian striatum, are described. Anatomical and neurochemical aspects of manipulations affecting behaviors related to S-R memory and reward correspond in certain respects to the features of these striatal compartments. These coincidences lead to an hypothesis concerning the function of the striatal compartments and their participation in neural systems controlling both immediate and learned behaviors.

Afferent Pathways↗
PubMed1989

Conditioned stereotypy: behavioral specification of the UCS and pharmacological investigation of the neural change.

Previous work has shown that conditioned stereotypy can be produced by repeated treatments with d-amphetamine or apomorphine. We replicated this phenomenon and found that, as in previous reports, the amplitude of conditioned stereotypy was about one-third that of the unconditioned stereotypy. On the basis of the hypothesis that the UCS in this conditioning situation is a specific stimulation level of dopamine receptors expressed as a peak behavioral effect (UCR), rats were exposed to the experimental boxes for a brief interval during the peak behavioral effect of the drugs. This procedure produced an amplitude of conditioned stereotypy about two-thirds that of unconditioned stereotypy. The issue of the synaptic mechanism mediating conditioned stereotypy was addressed by examining the effect of pimozide on the behavior. A dose of pimozide that completely blocked apomorphine-unconditioned stereotypy also blocked apomorphine-conditioned stereotypy with no sign of motor impairment. d-Amphetamine-conditioned stereotypy was not completely blocked by a dose of pimozide that completely blocked d-amphetamine-unconditioned stereotypy. The implications of these findings for understanding the neural basis of conditioned stereotypy are discussed.

Animals↗
PubMed1989

Memory facilitation produced by dopamine agonists: role of receptor subtype and mnemonic requirements.

The role of dopamine (DA) receptor subtypes in the acquisition of two memory tasks in the 8-arm radial maze was examined. The receptors were manipulated with posttraining, subcutaneous injections of an indirect DA receptor agonist (D-amphetamine), a selective D2 receptor agonist (LY171555), and a selective D1 receptor agonist (SKF-38393). On a win-stay task (sensitive to caudate nucleus lesions) a light cue signalled the location of food in 4 randomly selected arms on each trial. Rats were given one trial per day and injected after training on day 5. D-Amphetamine (2.0 mg/kg) and LY171555 (2.0 mg/kg) improved performance relative to controls; however SKF-38393 (1-4 mg/kg) had no effect on the acquisition of win-stay behavior. On a win-shift task (sensitive to fornix/hippocampal lesions) a delay of 18 hr was imposed between the first 4 and second 4 choices; drugs were injected after the first 4 choices. D-Amphetamine (1.0 mg/kg) and LY171555 (2.0 mg/kg) significantly improved retention relative to controls. SKF-38393 (1-4 mg/kg) had no effect on win-shift retention. These results suggest that the memory-improving properties of DA agonists on tasks sensitive to both hippocampal and caudate lesions are mediated by the D2 receptor.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Differential effects of fornix and caudate nucleus lesions on two radial maze tasks: evidence for multiple memory systems.

The present experiments were designed to examine the hypothesis that the mammalian brain contains anatomically distinct memory systems. Rats with bilateral lesions of caudate nucleus or fimbria-fornix and a control group were tested postoperatively on 1 of 2 versions of the radial maze task. In a standard win-shift version, each of the 8 arms of the maze was baited once, and the number of errors (revisits) in the first 8 choices of each trial was recorded. Fimbria-fornix rats were impaired in choice accuracy, while caudate animals were unimpaired relative to controls. Different groups of rats with similar lesions were tested on a newly developed win-stay version of the radial maze, in which the location of 4 randomly selected baited arms was signaled by a light at the entrance to each arm, and which required rats to revisit arms in which reinforcement had been previously acquired within a trial. Rats with fimbria-fornix lesions were superior to controls in choice accuracy on the win-stay radial maze task, while caudate animals were impaired relative to controls. The results demonstrate a double dissociation of the mnemonic functions of the hippocampus and caudate nucleus. Some implications of the presence of 2 memory systems in the mammalian brain are discussed.

Animals↗
PubMed1988

Effect of nigrostriatal dopamine depletion on the post-training, memory-improving action of amphetamine.

Systemic, post-training injections of d-amphetamine improve memory in a variety of learning situations. Evidence from self-stimulation and intra-striatal injection studies suggests that this effect may be a result of the amphetamine-promoted release of endogenous dopamine from nigro-striatal neurons. In the present study this hypothesis was supported by the demonstration that destruction of these neurons with intra-nigral injections of 6-hydroxydopamine eliminate the memory-improving effect of systemic, post-training injections of amphetamine.

Animals↗
PubMed1988

Effects of adrenal demedullation on the conditioned emotional response and on the memory improving action of glucose.

Results of previous experiments have demonstrated that posttraining, noncontingent ingestion of sucrose solutions, or injection of glucose solutions improve retention of various learning tasks. In the present experiment, we tested the hypothesis that this effect is due to a glucose-stimulated release of epinephrine from the adrenal medulla by testing the effect of posttraining glucose injections on retention of a conditioned emotional response (CER) in demedullated rats. In a preliminary experiment, demedullated rats were found to be deficient at acquiring the CER, but a similar deficit in sham-operated animals suggested that this was due to the surgical procedure rather than to the absence of the adrenal medulla. When appropriate shock parameters were used, posttraining glucose improved retention of the CER in a manner parallel to the effect of this treatment in normal rats. It was concluded that the memory improving effect of posttraining glucose does not involve an effect of this substance on the adrenal medulla.

Adrenal Medulla↗
PubMed1987

Effects of systemic and intracranial amphetamine injections on behavior in the open field: a detailed analysis.

Systemic injections of amphetamine result in profound changes in the behavior of animals in an open field. There is an increase in activity, certain species-typical behaviors are produced, and there is a tendency for any elicited behavior to be repeated in a stereotyped way. The present study examined the contributions of dopamine terminal regions to these effects in rats by microinjecting amphetamine directly into one of six discrete sites (medial frontal cortex, nucleus accumbens, anteromedial caudate nucleus, ventrolateral caudate nucleus, amygdala, or the region surrounding the area postrema) and making detailed behavioral observations. This data was compared with the behavior of systemically injected rats that were also observed in the open field. An observer recorded the occurrence of twelve categories of behavior and recorded photocell beam interruptions during five post-injection observation periods. The results confirmed and extended previous accounts of the behavior of systemically injected rats, adding increased snout contact with the environment as an additional effect of amphetamine. Intracranial injections produced changes in activity level from several of the injection sites but there was no increase in the species-typical behaviors associated with stereotypy. Changes in the occurrence of some recorded behaviors were produced by injections into most of the sites and these data are presented in detail.

Amphetamine↗
PubMed1987

Memory improvement by glucose, fructose, and two glucose analogs: a possible effect on peripheral glucose transport.

The memory-improving action of post-training, noncontingent injections of glucose was investigated in a series of experiments which examined the effects of several substances that interact with glucose metabolism on the retention of a conditioned emotional response and on blood glucose levels in male hooded rats. Although post-training glucose injections of 1, 2, and 3 g/kg all produced similar increases in blood glucose, only 2 g/kg improved retention, suggesting that attainment of a particular blood glucose level is not critical for memory improvement. Post-training injections of a range of insulin doses (0.25-4 IU/kg) failed to affect retention. Post-training injection of fructose (the same doses as were used for glucose) had no effect on blood glucose levels and, as with glucose, only the 2 g/kg dose improved retention. This finding suggests that blood glucose levels are not critical for the memory-improving effect, that glucose and fructose may act on the same substrate and, because fructose does not act directly on the brain, it raises the possibility that both substances act peripherally. Post-training injections of 2-deoxyglucose and 3-O-methylglucose both improved retention. The fact that these mostly nonmetabolized glucose analogs were effective suggests that the memory-improving action of glucose may depend on the activation of a membrane glucose transport mechanism. The implications of the possible action of glucose on peripheral transport mechanisms for understanding the effect of reinforcers on memory are discussed.

3-O-Methylglucose↗
PubMed1986

Effect of glucose on amphetamine-induced motor behavior.

The effect of 1 g/kg D-glucose on amphetamine-induced increases in activity; stereotypy; and rotation in rats with unilateral 6-OHDA lesions of nigro-striatal neurons was examined. The amphetamine dose-response curve for stereotypy was shifted to the right by glucose but retained the same slope as the control curve, suggesting that glucose competes for amphetamine or dopamine receptors that mediate this behavior. The slope of the dose-response curve for activity was significantly decreased by glucose, suggesting that glucose reduces activity levels in a manner that is non-competitive with the action of amphetamine or dopamine. Amphetamine-induced turning was unaffected by glucose at all doses tested. These data suggest that the effect of amphetamine on each of the three motor behaviors may be mediated by different dopamine-containing neurons, or by different post-synaptic dopamine receptors. The findings are also consistent with other data suggesting that glucose antagonizes dopamine function, but they suggest that this antagonism may not be uniform over all dopaminergic neurons or receptor types.

Amphetamine↗
PubMed1986

Anatomical disassociation of amphetamine's rewarding and aversive effects: an intracranial microinjection study.

Amphetamine has rewarding properties in some behavioral paradigms, such as self-administration and conditioned place preference (CPP), but an aversive component is also apparent when the drug is tested with the conditioned taste aversion (CTA) paradigm. The present study was an attempt to determine the neuroanatomical substrates of the drug's rewarding and aversive effects. Previous evidence suggested that amphetamine's stimulation of activity in dopaminergic synapses is critical for both effects. Amphetamine was therefore micro-injected bilaterally (10 micrograms/0.5 microliter per side) into six different dopaminergic sites, each in a different group of animals: the medial prefrontal cortex, nucleus accumbens, anteromedial caudate nucleus, lateroventral caudate nucleus, amygdala, and the region subjacent to the area postrema (AP region). The effects of these injections in both the taste and place conditioning paradigms were examined in separate experiments. Of the six sites, a significant CPP was observed only with accumbens injections and a significant CTA was observed only with AP region injections. It was concluded that the accumbens plays a primary role in mediating the rewarding effects of amphetamine and that the AP region plays a primary role in mediating the CTA. This constitutes an anatomical disassociation of amphetamine's rewarding and aversive effects. The differential associative bias of place-reward and taste-aversion learning apparent in the results is discussed.

Amygdala↗
PubMed1986

Contributions of dopamine terminal areas to amphetamine-induced anorexia and adipsia.

Systemic injections of amphetamine produce both anorexia and adipsia. Evidence suggests that it is the stimulation of activity by the drug in both noradrenergic and dopaminergic synapses that mediate these effects. The present study examined the contributions of dopamine terminal regions to these effects in rats by microinjecting amphetamine directly into one of six discrete sites (medial frontal cortex, nucleus accumbens, anteromedial caudate nucleus, ventrolateral caudate nucleus, amygdala, or the region surrounding the area postrema) and observing the effects of the injections on eating or drinking. The rats were mildly deprived of either food or water and following microinjection of either amphetamine or saline, were given access to food or water. Injections of amphetamine into either the nucleus accumbens or amygdala caused both anorexia and adipsia but no effects were observed from the other sites. It is suggested that the amphetamine's action on these two sites contributes to the anorexia and adipsia that are observed after systemic injection of the drug. Possible behavioral mechanisms for the effects are discussed.

Amphetamine↗
PubMed1986

Control of sensorimotor function by dopaminergic nigrostriatal neurons: influence on eating and drinking.

The literature on the effects of lesions of the lateral hypothalamic area (LHA) on eating and drinking is reviewed in an effort to understand the function of the neural substrate destroyed. The data suggest that damage to the dopaminergic nigrostriatal neurons that course through the LHA results in a decrease in sensorimotor facilitation; that is, an increase in the threshold for responding to stimuli that elicit orientation, approach and consumption. This increase results in decreased consumption of food and water. Evidence is also reviewed suggesting the possibility that striatal dopaminergic activity may mediate a negative feedback signal related to blood glucose level that influences responsiveness to food, and therefore eating. There is no evidence that the nigrostriatal system mediates a similar signal related to water balance and drinking. A second deficit associated with LHA lesions, caused by damage to the pallidofugal neurons that descend through this area, is a dysfunction of motor control of the head and mouth. This results in an increase in the effort required to consume food and water, also leading to decreased consumption. These two behavioral factors: an increased threshold for responding to the sensory properties of food and water and an increase in the effort required to eat and drink are used to explain the symptoms making up the lateral hypothalamic syndrome without postulating changes in physiological regulatory (set point) mechanisms.

Animals↗