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Journal ArticleDOI

Semistarvation-induced hyperactivity compensates for decreased norepinephrine and dopamine turnover in the mediobasal hypothalamus of the rat.

01 Jan 1990-Journal of Neural Transmission (Springer-Verlag)-Vol. 79, Iss: 1, pp 113-124
TL;DR: The combined influence of semistarvation and hyperactivity on central catecholamine turnover in the rat is discussed as an animal model for the effects of malnutrition and heavy exercise often observed in anorexia nervosa.
Abstract: Male Wistar rats were housed in running wheel cages and were restricted in their food intake, in order to reduce the initial body weight by 30% within 10 days. Rats increased their daily running up to distances between 7 and 11 km compared to the maximum 2.5 km in controls fed ad libitum. The hypothalamic noradrenaline (NE) turnover, as estimated by the concentration of the major metabolite MHPG, was significantly decreased in semistarved sedentary rats compared to controls. Hyperactivity resulted in marked elevation of NE turnover at all time points examined. Semistarvation-induced decreases of dopamine (DA) turnover as estimated by the concentrations of its major metabolite DOPAC, could also be compensated by hyperactivity. The circadian pattern of NE turnover parallels the pattern of running activity. MHPG levels at times of high activity were even higher than in controls fed ad libitum (p<0.01). The availability of the precursor tyrosine, as indicated by the ratio of plasma tyrosine to the large neutral amino acids, was significantly decreased in semistarvation (p<0.0001); hyperactivity caused a further decrease (p<0.001), indicating that tyrosine availability is not, under these conditions, a limiting factor for noradrenaline turnover. The combined influence of semistarvation and hyperactivity on central catecholamine turnover in the rat is discussed as an animal model for the effects of malnutrition and heavy exercise often observed in anorexia nervosa.
Citations
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Journal ArticleDOI
TL;DR: The results of the first studies using microdialysis and voltammetry indicate that the release of most neurotransmitters is influenced by exercise, which indicates that a further understanding of the effects of exercise on brain neurotransmission can be gained.
Abstract: Physical exercise influences the central dopaminergic, noradrenergic and serotonergic systems. A number of studies have examined brain noradrenaline (norepinephrine), serotonin (5-hydroxytryptamine; 5-HT) and dopamine with exercise. Although there are great discrepancies in experimental protocols, the results indicate that there is evidence in favour of changes in synthesis and metabolism of monoamines during exercise. There is a possibility that the interactions between brain neurotransmitters and their specific receptors could play a role in the onset of fatigue during prolonged exercise. The data on the effects of branched chain amino acid (BCAA) supplementation and 'central fatigue' seem to be conflicting, although recent studies suggest that BCAA supplementation has no influence on endurance performance. There are numerous levels at which central neurotransmitters can affect motor behaviour; from sensory perception, and sensory-motor integration, to motor effector mechanisms. However, the crucial point is whether or not the changes in neurotransmitter levels trigger or reflect changes in monoamine release. Until recently most studies were done on homogenised tissue, which gives no indication of the dynamic release of neurotransmitters in the extracellular space of living organisms. Recently, new techniques such as microdialysis are voltammetry were introduced to measure in vivo release of neurotransmitters. Microdialysis can collect virtually any substance from the brain of a freely moving animal with a limited amount of tissue trauma. This method allows measurement of local neurotransmitter release during on-going behavioural changes such as exercise. The results of the first studies using these methods indicate that the release of most neurotransmitters is influenced by exercise. Although the few studies that have been published to date show some discrepancies, we feel that these recently developed and more sophisticated in vivo methods will improve our insight into the relationship between the monoamine and other transmitters during exercise. Continued quantitative and qualitative research needs to be conducted so that a further understanding of the effects of exercise on brain neurotransmission can be gained.

447 citations

Journal ArticleDOI
TL;DR: It is found that chronic activity wheel running increased NE levels in the pons medulla at rest and protected against NE depletion in locus coeruleus cell bodies after footshock; the concomitant reduction in escape-latency was consistent with an antidepressant effect.
Abstract: This paper summarizes our studies examining whether changes in levels of brain monoamines after chronic exercise are associated with altered behavioral and endocrine responses to stressors other than exercise. The focus is on using animal models relevant for understanding reports by humans that regular physical activity reduces depression and anxiety. We studied the effects of chronic activity wheel running or treadmill exercise training on levels of norepinephrine (NE) measured in brain cell bodies and terminal regions at rest and after behavioral stress. We also measured brain levels of serotonin, i.e., 5-hydroxytryptamine (5-HT), dopamine (DA), and gamma aminobutyric acid (GABA), which function as both antagonists and synergists with NE. In general, we found that chronic activity wheel running increased NE levels in the pons medulla at rest and protected against NE depletion in locus coeruleus cell bodies after footshock; the concomitant reduction in escape-latency was consistent with an antidepressant effect. Wheel running also decreased the density of GABAA receptors in the corpus striatum while increasing open-field locomotion, consistent with an anxiolytic effect, but had no effect on hypothalamic-pituitary-adrenal cortical response to footshock measured by plasma levels of adrenocorticotropic hormone (ACTH), corticosterone, and prolactin. In contrast, treadmill exercise training increased the metabolism of NE in brain ascending terminal areas for NE, increased the secretion of ACTH after footshock and immobilization stress and had no effect on GABAA receptor density or open field locomotion. The validity of animal models for studying depression and anxiety after forced versus voluntary exercise is discussed. Recommendations are offered for improving the methods used in this area of research.

284 citations

Journal ArticleDOI
TL;DR: Hypoleptinemia, as a result of the food restriction, may represent the initial trigger for the increased activity levels in AN patients and in food-restricted rats.

242 citations


Cites background from "Semistarvation-induced hyperactivit..."

  • ...Whereas many studies have applied the original restricted feeding paradigm described above, SIH can also be induced in rats exposed to running wheels and restricted to 60–75% of their previous ad libitum food intake [10,47,79,94,95]....

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  • ...[94] Broocks A, Liu J, Pirke KM....

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Journal ArticleDOI
TL;DR: A supervised exercise program by which overactivity may be addressed specifically in the treatment of anorexia nervosa patients is proposed.
Abstract: A relationship between starvation and hyperactivity has been observed in animal models, in experiments with human subjects, and in dieting disorder patients. Since the earliest descriptions of anorexia nervosa, excessive physical activity has figured prominently as a symptom of the illness, yet little attention has been directed towards this phenomenon. The aims of this paper are to review the published literature, to report our experience of the role of physical overactivity in the clinical presentation of dieting disorders, to discuss its implications for treatment, and to propose a supervised exercise program by which overactivity may be addressed specifically in the treatment of these patients.

208 citations

Journal ArticleDOI
TL;DR: T treadmill exercise training is accompanied by brain noradrenergic adaptations consistent with increased metabolism of NE in areas containing NE cell bodies and ascending terminals, whereas treadmill running and wheel running are accompanied by increases in levels ofNE in the areas of NEcell bodies and the spinal cord, independently of an exercise training effect.
Abstract: Regional changes in concentrations of brain norepinephrine [NE] and its metabolites after chronic exercise have not been described for exercise protocols not confounded by other stressors. We examined levels of [NE], 3-methoxy-4-hydroxyphenylglycol [MHPG], and 3,4-dihydroxyphenylglycol [DHPG] in the frontal cortex, hippocampus, pons-medulla, and spinal cord after 8 wk of exercise. Male Sprague-Dawley rats (N = 36) were randomly assigned to three conditions: 1) 24-h access to activity wheel running (WR), 2) treadmill running (TR) at 0 degrees incline for 1 h.d-1 at 25-30 m.min-1, or 3) a sedentary control group (C). Levels (nmol.g-1) of [NE], [MHPG], and [DHPG] were assayed by high performance liquid chromatography with electrochemical detection. Planned contrasts (P < 0.05) indicated that exercise training increased succinate dehydrogenase activity (mmol cytochrome C reduced.min-1.g-1 wet weight) in soleus muscle for TR compared with WR or C. [NE] was higher in the pons-medulla and spinal cord for both TR and WR compared with C. [DHPG] was higher in the pons-medulla for TR compared with C, and [MHPG] was higher in the frontal cortex and in the hippocampus for TR compared with C. Our results suggest that treadmill exercise training is accompanied by brain noradrenergic adaptations consistent with increased metabolism of NE in areas containing NE cell bodies and ascending terminals, whereas treadmill running and wheel running are accompanied by increases in levels of NE in the areas of NE cell bodies and the spinal cord, independently of an exercise training effect.

168 citations

References
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Journal Article
TL;DR: This relationship allows precursor administration to produce selective physiologic effects by enhancing neurotransmitter release from some but not all of the neurons potentially capable of utilizing the precursor for this purpose, and allows the investigator to predict when administering the precursor might be useful for amplifying a physiologic process, or for treating a pathologic state.
Abstract: Studies performed during the past decade have shown that the rates at which certain neurons produce and release their neurotransmitters can be affected by precursor availability, and thus by the changes in plasma composition that occur after ingestion of the precursors in purified form or as constituents of foods. Thus, tryptophan administration or a plasma ratio of tryptophan to other large neutral amino acids, thereby raising brain tryptophan levels, increasing the substrate saturation of tryptophan hydroxylase, and accelerating the synthesis and release of serotonin. Tyrosine administration or a high-protein meal similarly elevates brain tyrosine and can accelerate catecholamine synthesis in the CNS and sympathoadrenal cells, while the consumption of lecithin or choline increases brain choline levels and neuronal acetylcholine synthesis. The physiologic and biochemical mechanisms that must exist in order for nutrient consumption to affect neurotransmitte synthesis have been characterized and include: 1) the lack of significant feedback control of plasma levels of the precursor; 2) the lack of a real "bloodbrain barrier" for the precursor, i.e. the ability of the plasma level of the precursor to control its influx into, or efflux from, the CNS; 3) the existence of a low-affinity (and thus unsaturated) transport system mediating the flux of the precursor between blood and brain; 4) low-affinity kinetics for the enzyme that initiates the conversion of the precursor to the transmitter; and, 5) the lack of end-product inhibition of the enzyme, in vivo, by its ultimate product, the neurotransmitter. The extent to which neurotransmitter synthesis in any particular aminergic neuron happens to be affected by changes in the availability of its precursor probably varies directly with the neuron's firing frequency. This relationship allows precursor administration to produce selective physiologic effects by enhancing neurotransmitter release from some but not all of the neurons potentially capable of utilizing the precursor for this purpose. It also allows the investigator to predict when administering the precursor might be useful for amplifying a physiologic process, or for treating a pathologic state. (for example, tyrosine administration raises blood pressure in hypotensive rats, lowers it in hypertensive animals, and has little effect on blood pressure in normotensive animals; the elevation in blood pressure probably reflects enhanced catecholamine release from sympathoadrenal cells, while the reduction in hypertensive animals probably results from increased catecholamine release within the brain-stem.) Such predictions are now being tested clinically in many institution. Available evidence suggests that lecithin or cholie administration can diminish the frequency of abnormal movements in patients with tardive dyskinesia...

644 citations

Journal ArticleDOI
TL;DR: The role of catecholamines in the regulation of metabolic processes has been recognized for over 50 years and they are known to influence metabolism in two major ways: they increase the rate of cel...
Abstract: THE importance of catecholamines in the regulation of metabolic processes has been recognized for over 50 years. Catecholamines influence metabolism in two major ways: they increase the rate of cel...

474 citations

Book
01 Jan 1922

405 citations


Additional excerpts

  • ...This corresponds with earlier observations (Richter, 1922), demonstrating that the time of feeding has a more powerfull "Zeitgeber" function, when food intake is restricted than the light-dark cycle....

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Journal ArticleDOI
TL;DR: It is suggested that deamination, reduction, and subsequent conjugation with sulfate is the primary route of metabolism of normetanephrine in rat brain and that norepinephrine is also metabolized to this sulfate conjugate.

352 citations