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At least 667 records · Page 37Linked to original sources
PubMed1999

Post-session intra-perifornical region quinpirole infusions retard the consolidation of an appetitive differential conditioning task.

We have shown previously that post-session infusions of the D2/D3 dopamine receptor antagonist sulpiride within the perifornical region of the lateral hypothalamus (PFH) greatly facilitated the acquisition of an appetitive differential conditioning task. Here, we have examined the effects of the D2/D3 dopamine receptor agonist quinpirole on acquisition of this task. Conditioning sessions consisted of an initially neutral stimulus (CS+) preceding availability of a 10% sucrose reward (US), and a control stimulus (CS-), never associated with the US, were presented, followed by bilateral intra-PFH infusions of quinpirole (0, 0.1, 10 nmol). The acquisition of a conditioned approach response during the CS+ period was impaired by quinpirole administration in a dose-dependent manner. No other behavioural measure was affected. All groups subsequently acquired the conditioned approach response, following cessation of the post-session infusion procedure. The present data extends previous findings, suggesting that the level of activation of dopamine receptors in the vicinity of the PFH significantly influences the consolidation of appetitive Pavlovian associations.

Animals↗
PubMed2005

Endocannabinoids in the regulation of appetite and body weight.

The discovery of cannabinoid receptors, together with the development of selective cannabinoid receptor antagonists, has encouraged a resurgence of cannabinoid pharmacology. With the identification of endogenous agonists, such as anandamide, scientists have sought to uncover the biological role of endocannabinoid systems; initially guided by the long-established actions of cannabis and exogenous cannabinoids such as delta9-tetrahydrocannabinol (THC). In particular, considerable research has examined endocannabinoid involvement in appetite, eating behaviour and body weight regulation. It is now confirmed that endocannabinoids, acting at brain CB1 cannabinoid receptors, stimulate appetite and ingestive behaviours, partly through interactions with more established orexigenic and anorexigenic signals. Key structures such as the nucleus accumbens and hypothalamic nuclei are sensitive sites for the hyperphagic actions of these substances, and endocannabinoid activity in these regions varies in relation to nutritional status and feeding expression. Behavioural studies indicate that endocannabinoids increase eating motivation by enhancing the incentive salience and hedonic evaluation of ingesta. Moreover, there is strong evidence of an endocannabinoid role in energy metabolism and fuel storage. Recent developments point to potential clinical benefits of cannabinoid receptor antagonists in the management of obesity, and of agonists in the treatment of other disorders of eating and body weight regulation.

Animals↗
PubMed2004

Appetite regulatory neuropeptides are expressed in the sheep hypothalamus before birth.

In the adult, a hypothalamic neural network acts to maintain energy balance in response to nutritional feedback from the periphery. Although there is an immediate requirement for this system to be functional at birth, it is unknown whether the components of this central neural network are expressed in the developing brain before birth. We therefore examined in the fetal sheep hypothalamus during late gestation gene expression for leptin receptor (OB-Rb) and neuropeptides that regulate energy balance in the adult. Brains were collected from fetal sheep at 110 days (n = 12) and 140 days of gestation (n = 5) (term = 150 days) and gene expression was detected in all hypothalami using in situ hybridization with radiolabelled riboprobes for OB-Rb, neuropeptide Y (NPY), agouti-related peptide, pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript (CART). All mRNAs were expressed in the arcuate nucleus of fetuses at both time points. Additional sites of mRNA expression were the dorsomedial hypothalamus (DMH) for NPY, the paraventricular nucleus (PVN), ventromedial hypothalamus (VMH) and lateral hypothalamic area for CART, and the DMH, PVN and VMH for OB-Rb. We have therefore demonstrated that adult-like localization of gene expression for OB-Rb and key appetite regulatory neuropeptides is established in the ovine hypothalamus before birth. Thus, the fetus possesses a central appetite regulatory neural network with the potential to respond to changes in nutrient supply, which could impact on energy balance regulation both before and after birth.

Age Factors↗
PubMed2004

Neural contributions to the motivational control of appetite in humans.

The motivation to eat in humans is a complex process influenced by intrinsic mechanisms relating to the hunger and satiety cascade, and extrinsic mechanisms based on the appetitive incentive value of individual foods, which can themselves induce desire. This study was designed to investigate the neural basis of these two factors contributing to the control of motivation to eat within the same experimental design using positron emission tomography. Using a novel counterbalanced approach, participants were scanned in two separate sessions, once after fasting and once after food intake, in which they imagined themselves in a restaurant and considered a number of items on a menu, and were asked to choose their most preferred. All items were tailored to each individual and varied in their incentive value. No actual foods were presented. In response to a hungry state, increased activation was shown in the hypothalamus, amygdala and insula cortex as predicted, as well as the medulla, striatum and anterior cingulate cortex. Satiety, in contrast, was associated with increased activation in the lateral orbitofrontal and temporal cortex. Only activity in the vicinity of the amygdala and orbitofrontal cortex was observed in response to the processing of extrinsic appetitive incentive information. These results suggest that the contributions of intrinsic homeostatic influences, and extrinsic incentive factors to the motivation to eat, are somewhat dissociable neurally, with areas of convergence in the amygdala and orbitofrontal cortex. The findings of this study have implications for research into the underlying mechanisms of eating disorders.

Adult↗
PubMed2005

A single time-window for protein synthesis-dependent long-term memory formation after one-trial appetitive conditioning.

Protein synthesis is generally held to be essential for long-term memory formation. Often two periods of sensitivity to blockade of protein synthesis have been described, one immediately after training and another several hours later. We wished to relate the timing of protein synthesis-dependence of behavioural long-term memory (LTM) formation to an electrophysiological correlate of the LTM memory trace. We used the snail Lymnaea because one-trial appetitive conditioning of feeding using a chemical conditioned stimulus leads to a stable LTM trace that can be monitored behaviourally and then electrophysiologically in preparations made from the same animals. Anisomycin (an inhibitor of translation) injected 10 min after training blocked behavioural LTM formation. Actinomycin D (an inhibitor of transcription) was also effective at 10 min. When anisomycin, at doses shown to be effective in blocking central nervous system protein synthesis, was injected at 1, 2, 3, 4, 5 and 6 h after training there was no effect on recall. These results indicate that there is a single period of sensitivity to protein synthesis inhibition in Lymnaea lasting for between 10 min and 1 h after training with no evidence for a second window of sensitivity. An electrophysiological correlate of LTM was found to be sensitive to anisomycin injected 10 min after training. It is unusual to find only one period of protein synthesis-dependence in detailed time-course studies of LTM, and this suggests that the consolidation processes involving protein synthesis are relatively rapid in one-trial appetitive conditioning and complete within 1 h of training.

Analysis of Variance↗
PubMed2006

The infralimbic cortical area commands the behavioral and vegetative arousal during appetitive behavior in the rat.

The infralimbic cortical area is a good candidate to send processed motivational signals to initiate the arousing and autonomic responses that characterize appetitive behaviors. To test this hypothesis we enticed hungry rats with food while assessing locomotion (as an index of arousal level) and temperature responses, and evaluated Fos immunoreactivity (IR) in the infralimbic area and in subcortical nuclei involved in thermoregulation or arousal. We also recorded from single infralimbic neurons in freely moving rats while enticing them with food. We found that 83% of infralimbic neurons were excited or inhibited by feeding and, in particular, that 33% of infralimbic neurons increased their discharge rate during food enticing. Intact rats showed increased Fos IR in the infralimbic area, as well as in many other cortical areas. The excitotoxic lesion of the infralimbic cortex abolished the arousing and hyperthermic responses observed in intact rats, as well as the expression of Fos IR in the ascending arousal system and subcortical thermoregulatory regions. We conclude that the infralimbic area plays a central role in implementing behavioral arousing and thermal responses during an appetitive behavior.

Animals↗
PubMed2006

Physical and emotional development, appetite and body image in adolescents who failed to thrive as infants.

BACKGROUND: Previous studies suggest that failure to thrive in infancy may be associated with adverse sequelae in childhood. Although cognitive abilities have been extensively investigated, little systematic research is available on other aspects of development. METHODS: Eighty-nine children who failed to thrive as infants and 91 controls were followed up when twelve years old and examined using anthropometric measurement, self-ratings of appetite and body image, the Dutch Eating Behaviour Questionnaire, the Self-perception Profile for Children, The Revised Children's Manifest Anxiety Scale, the parent and child form of the Mood and Feelings Questionnaire and the parent and teacher's form of the Child Behavior Checklist. RESULTS: The children who failed to thrive were significantly shorter and lighter at twelve and had significantly lower BMIs, but they did not go into puberty any later. They were more likely to rate their appetite as lower than their best friend's, were generally more satisfied with their body shape, and had significantly lower restraint score on the Dutch Eating Behaviour Questionnaire. They were not significantly different from controls on any of the measures reflecting anxiety, depression or low self-esteem. CONCLUSIONS: Failure to thrive in infancy is not associated with adverse emotional development in childhood.

Anthropometry↗
PubMed2005

Animal models of programming: early life influences on appetite and feeding behaviour.

Epidemiological observations of associations between early life nutrition and long-term disease risk have prompted detailed experimental investigation of the biological basis of programming. Studies using rodent or large animal models have clearly established the biological plausibility of nutritional programming and are now yielding important information on underlying mechanisms. Nutritional interventions in pregnancy, including global food restriction, protein restriction, micronutrient restriction and excess fat feeding, determine a consistent cluster of disorders in the resulting offspring. The common association of such diverse nutritional disturbances with hypertension, glucose intolerance and adiposity suggests that a small number of simple common mechanisms are active in response to fetal nutrient imbalance. Studies of rodent models indicate that fetal undernutrition determines adult adiposity. It is unclear whether the increase in central adiposity is related to increased food intake or reduced energy expenditure, although evidence exists to suggest that both may act together. Rats subject to intrauterine protein restriction exhibit increased preference for high fat foods. Feeding of energy dense foods to rats that were undernourished in utero promotes a greater degree of obesity than is noted in animals subject to adequate nutrition in fetal life. There is evidence to suggest that programming of appetite may stem from remodelling of hypothalamic structures that control feeding and programming of the expression of genes involved in responses to orexogenic hormones. The early life programming of appetite and obesity is a complex phenomenon and our understanding of how maternal nutrition determines later energy balance is at a very early stage.

Adipose Tissue↗
PubMed2005

How palatable food disrupts appetite regulation.

Appetite regulation is part of a feedback system that controls the energy balance, involving a complex interplay of hunger and satiety signals, produced in the hypothalamus as well as in peripheral organs. Hunger signals may be generated in peripheral organs (e.g. ghrelin) but most of them are expressed in the hypothalamus (neuropeptide Y, orexins, agouti-related peptide, melanin concentrating hormone, endogenous opiates and dopamine) and are expressed during situations of energy deficiency. Some satiety signals, such as cholecystokinin, glucagon-like peptide 1, peptide YY and enterostatin are released from the digestive tract in response to food intake. Others, such as leptin and insulin, are mobilized in response to perturbations in the nutritional state. Still others are generated in neurones of the hypothalamus (alpha-melanocyte-stimulating hormone and serotonin). Satiety signals act by inhibiting the expression of hunger signals and/or by blunting their effect. Palatable food, i.e. food rich in fat and sugar, up-regulates the expression of hunger signals and satiety signals, at the same time blunting the response to satiety signals and activating the reward system. Hence, palatable food offsets normal appetite regulation, which may explain the increasing problem of obesity worldwide.

Animals↗
PubMed1987

Sodium appetite as well as 24-h variations of fluid balance, mean arterial pressure and heart rate in spontaneously hypertensive (SHR) and normotensive (WKY) rats, when on various sodium diets.

Young SHR and WKY rats were compared, first, concerning sodium (Na) appetite during 'rest', mild social stress and ACTH injections, second, concerning the diurnal patterns of water intake, urine output, mean arterial pressure (MAP) and heart rate (HR) while on various Na diets: 0.5 mmol Na(LNa), 5 or 12-13 mmol Na (CNa), 50 (HNa) or 120 mmol Na (vHNa) per 100 g food. Sodium appetite and water intake were about 50% higher in SHR than in WKY (4-4.5 vs 2.5-3 mmol Na per 100 g body wt day-1). It was modestly increased by both social stress and ACTH, and more so in WKY, thereby approaching that in SHR. Concerning the various Na diets and their influences, daytime resting MAP was modestly lowered in LNaSHR and slightly increased in vHNaSHR compared with CNaSHR but largely equal in all WKY groups. Food-water consumption was concentrated to the active night period, but even high Na-water intakes caused no signs of sustained hypervolaemia, because each intake bout was in both SHR and WKY eliminated by urine within 30-40 min. However, particularly the vHNa diet in SHR also increased the frequency of drinking, and each bout caused transient, evidently neurogenic MAP and HR increases which occurred too rapidly to be consequences of blood volume expansion. As a result, the diurnal MAP-HR patterns in SHR varied markedly with the Na diets, in vHNa group resulting in considerably raised average diurnal MAP levels even though resting daytime MAP was here nearly the same as in CNaSHR. These findings illustrate how largely continuous diurnal recordings are needed to judge correctly the relationships between, for example, Na intake, volume equilibrium and MAP. Finally, the relevance of these results in rats for also judging the control of Na balance in man is discussed.

Animals↗
PubMed1990

Serotonin and appetite.

Feeding or food withdrawal can affect the supply of tryptophan to the brain and hence (in some circumstances) 5-HT synthesis therein. Also fenfluramine which releases 5-HT to postsynaptic receptors suppresses appetite, and there are reports that tryptophan can have a similar effect. Furthermore, feeding is reported to release hypothalamic 5-HT. Therefore 5-HT could have a role in the normal termination of feeding and perhaps also in disorders of appetite. The recognition of various 5-HT receptor subtypes has stimulated research in this area. We have now investigated the involvement of the subtypes in the pharmacological control of feeding. Thus, 5-HT1A agonists (8-OHDPAT, buspirone, gepirone, etc.) stimulate intake in freely feeding rats, probably by activating autoreceptors on the cell bodies of 5-HT neurons so that 5-HT release at terminals is decreased. The hyperphagia is not explicable by increased activity or gnawing and is strikingly manifest against carbohydrate in carbohydrate vs. protein choice experiments. Feeding in previously food-deprived rats is decreased by the 5-HT agonists RU 24969, 1-(3-chlorophenyl) piperazine (mCPP) and 1-(3-trifluoromethyl) phenyl) piperazine (TFMPP). Effects of antagonists on these properties suggest that RU 24969-induced hypophagia depends on 5-HT1B receptors only, while mCPP and TFMPP induce hypophagia at 5-HT1C sites, though this effect also requires 5-HT1B receptors for its expression. Responsible sites occur in the paraventricular nucleus of the hypothalamus as infusing either RU 24969 or TFMPP therein causes hypophagia. On systemic injection, the hypophagic drugs are particularly active in female rats, an effect of conceivable relevance to human anorexic illness.

Animals↗
PubMed1998

Neuroendocrine interactions between galanin, opioids, and neuropeptide Y in the control of reproduction and appetite.

Galanin is a pleiotropic neuroendocrine signal produced in discrete subpopulations of neurons distributed in several sites in the hypothalamus. Neuropeptide Y and beta-endorphin also display pleiotropism, but they are produced by subpopulations of neurons located only in the arcuate nucleus of the hypothalamus. Each of these neuropeptides exerts a regulatory influence on reproduction and appetitive behavior. Experimental and morphologic evidence from our laboratory show direct contacts and interplay among these diverse signals. Seemingly, an interconnected network composed of these three neuropeptide-producing neurons provides precision and site specificity in the relay of information necessary to govern reproduction and appetite. Disruptions in this interplay are likely to manifest in untoward consequences such as infertility and obesity.

Animals↗
PubMed1999

The role of brain-gut peptides in the control of sodium appetite.

Ingestion of food and fluid stimulates release of a number of peptides from the gastrointestinal system. These peptides are recognized to act as neurotransmitters/neuromodulators and act at both peripheral and central receptors. Many studies indicate that these peptides are important signals in terminating meals. Recent studies suggest that bombesin, a peptide related to gastrin-releasing peptide, suppresses sodium appetite. We have investigated the role of cholecystokinin (CCK) in the control of sodium appetite. Our studies indicate that CCK is effective at reducing saline intake. We found that exogenous, intraperitoneal CCK octapeptide suppresses saline intake. Moreover, administration of trypsin inhibitor to stimulate endogenous CCK release resulted in suppression of saline intake. Finally, intraperitoneal administration of the CCK receptor antagonist lorglumide resulted in increased saline intake. These observations extend the potential role of gastrointestinal peptides in the modulation of ingestive behavior.

Animals↗
PubMed1999

The extended amygdala and salt appetite.

Both chemo- and mechanosensitive receptors are involved in detecting changes in the signals that reflect the status of body fluids and of blood pressure. These receptors are located in the systemic circulatory system and in the sensory circumventricular organs of the brain. Under conditions of body fluid deficit or of marked changes in fluid distribution, multiple inputs derived from these humoral and neural receptors converge on key areas of the brain where the information is integrated. The result of this central processing is the mobilization of homeostatic behaviors (thirst and salt appetite), hormone release, autonomic changes, and cardiovascular adjustments. This review discusses the current understanding of the nature and role of the central and systemic receptors involved in the facilitation and inhibition of thirst and salt appetite and on particular components of the central neural network that receive and process input derived from fluid- and cardiovascular-related sensory systems. Special attention is paid to the structures of the lamina terminalis, the area postrema, the lateral parabrachial nucleus, and their association with the central nucleus of the amygdala and the bed nucleus of the stria terminalis in controlling the behaviors that participate in maintaining body fluid and cardiovascular homeostasis.

Amygdala↗
PubMed2002

Appetite suppressants as agonist substitution therapies for stimulant dependence.

Several lines of evidence support a dual-deficit model of stimulant withdrawal in which decreases in synaptic dopamine (DA) and serotonin (5-HT) contribute to withdrawal symptoms, drug craving, and relapse. According to the dual-deficit model, DA dysfunction during withdrawal underlies anhedonia and psychomotor disturbances, whereas 5-HT dysfunction gives rise to depressed mood, obsessive thoughts, and lack of impulse control. The model suggests that medications capable of normalizing stimulant-induced DA and 5-HT deficits should be effective treatment adjuncts. Furthermore, the model may explain why medications targeting only one neurotransmitter system (i.e., DA) have failed to treat cocaine dependence. Amphetamine-type appetite suppressants are logical choices for neurochemical normalization therapy of stimulant dependence, yet few clinical studies have tested anorectics in this regard. The chief purpose of the present work is to profile the activity of various anorectic agents at DA, 5-HT, and NE transporters, in order to identify possible medications for stimulant dependence. Compounds were tested in vitro for their ability to stimulate release and inhibit uptake of [(3)H]DA, [(3)H]NE, and [(3)H]5-HT. Selected compounds were tested in vivo for their ability to elevate extracellular levels of DA and 5-HT in rat nucleus accumbens. The results show that clinically available appetite suppressants display a wide range of activities at monoamine transporters. However, no single medication possesses equal potency at DA and 5-HT transporters, suggesting that none of the anorectics is ideally suited for treatment of stimulant addictions. Future efforts should focus on developing new medications that possess the desired therapeutic activity but lack the adverse effects associated with older amphetamine-type anorectics.

Aminorex↗
PubMed1995

Intense sweeteners and the control of appetite.

The sensation of sweet taste without calories has been said to increase appetite and promote food consumption. Regular use of intense sweeteners might therefore lead to a paradoxical weight gain. These alarmist reports have not been confirmed by recent experimental data. There is no evidence that the addition of an intense sweetener to a plain stimulus promotes appetite or results in increased food consumption during some later meal. While replacing sugars with intense sweeteners (with attendant decrease in energy) has been said to result in energy compensation, published studies have variously reported perfect compensation, partial compensation, or no compensation at all, depending on the conditions used. Longer-term studies are needed to assess chronic effects of intense sweeteners on dietary compliance and the control of body weight.

Adaptation, Physiological↗
PubMed1979

The metabolic effects of sodium depletion in calves on salt appetite assessed by operant methods.

1. Sodium deficiency was induced in calves by unilateral exteriorization of the parotid duct, the continual loss of alkaline saliva from the body to the environment causing negative sodium balance. 2. The metabolic effect of negative sodium balance was seen in statistically significant reduction in plasma sodium and blood bicarbonate, together with marked acidosis and reduced plasma osmolality. 3. The homoeostatic response to sodium depletion was associated with a reversal of sodium/potassium ratio in parotid saliva and a reduction of the rate of secretion. Appetite diminished. The extracellular fluid was halved as marked diuresis developed with considerable weight loss. Urinary and faecal sodium was reduced to zero. 4. On restoration of sodium balance by allowing the calves to drink sodium bicarbonate solutions the metabolic deviations were eliminated. 5. During sodium depletion the parotid gland was able to respond to transient reflex stimulation by increasing flow rate and the sodium concentration of the saliva. 6. When sodium depleted, the calves became restless and agitated and would run from the home pen to the operant procedure stand. The sodium depleted animals readily pressed a panel for sodium bicarbonate rewards in direct proportion to the degree of sodium imbalance. When the balance was restored the motivation to work for sodium bicarbonate disappeared. 7. The motivation which developed during sodium depletion was directed specifically towards the sodium ion. Lithium was an exception to this rule and sodium carbonate was aversive. 8. It is possible that in sodium depletion the glottal sodium taste receptors develop an enhanced threshold for sodium ions because of the reduced sodium content of the saliva. This effect would be abolished when the content of sodium was restored in saliva. 9. The correlation of operant reactions and sodium depletion suggests that the consequential metabolic effects activate changes in the central nervous system. 10. The metabolic changes which develop in parallel with the severity of the sodium deficit appear to be able to evoke behavioural changes with increase in salt appetite directed towards restoration of sodium balance.

Animals↗
PubMed1992

Correlation between echographic gastric emptying and appetite: influence of psyllium.

The correlation between ultrasonographic gastric emptying and appetite was studied. Echographic evaluation of gastric emptying by measurement of the antral vertical diameter and assessment of sensations of hunger and satiety using analogue visual scales were performed simultaneously in 12 healthy volunteers. Measurements were carried out after the intake of 10.8 g psyllium or placebo in a randomised, crossover, double blind trial. The correlation between echographic gastric emptying and sensations of hunger and satiety was excellent (p < 0.001) after the intake of either psyllium or placebo. Psyllium significantly delayed gastric emptying from the third hour after a meal. It increased the sensation of satiety and decreased hunger at the sixth hour after the meal. The association between echographic measurement and visual scales is a simple method of evaluating the relationship between the stomach and appetite. The pharmacodynamic effect of psyllium should be confirmed by longterm therapeutic trials.

Adolescent↗