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Measuring the appetitive strength of ethanol: use of an extinction trial procedure.

Assessing the motivational level related to gaining access to ethanol (appetitive strength) is critical in understanding the human behavioral processes described as "craving." Use of an animal model that separates the behavior required to obtain the opportunity to consume ethanol from the actual consumption allows for independent measures of appetitive strength that are not intermixed with the effects of the consumed ethanol. In this model, two different methods have been applied to determine the appetitive strength: an across-sessions breakpoint procedure and single-session extinction trials. Although both methods provide an estimate of appetitive strength, the current studies were performed to provide some comparison between them. From the results and comparison with findings from prior studies, it was determined that the breakpoint procedure gave the most stable and potentially least influenced measure of appetitive strength. On the other hand, extinction trials in general provided a stable measure, somewhat different from breakpoint, that could be influenced by behavioral effects other than those related to ethanol consumption. Ethanol intakes were in a pharmacologically relevant range, averaging approximately 1.0 g/kg during 20 min of access to the solutions. Both the breakpoint and extinction measures provide additional evidence of a separation between the behavioral processes of ethanol seeking and ethanol drinking, as there was no relation between lever-press responding and ethanol intake. Thus, when choosing a method, it is possible to assess the appetitive strength of ethanol. However, care should be exercised to avoid misinterpretation of results.

Alcohol Drinking↗

Appetitive conditioning: neural bases and implications for psychopathology.

Appetitive conditioning is the process through which new rewards are learned and acquire their motivational salience. Although it has the same evolutionary survival significance as aversive conditioning, appetitive conditioning has rarely been studied in humans. This gap may be explained by the difficulty to find in humans suitable appetitive stimuli that can elicit physiological responses similar to those elicited by aversive stimuli. To help remedy this gap, we review the literature on conditioning, with emphasis on appetitive conditioning. This review comprises three parts. First, we examine the different forms of conditioning. Second, we review the neural basis of appetitive conditioning, particularly from a functional neuroimaging perspective. And third, we demonstrate how perturbations in processes involved in appetitive conditioning can contribute to implicated psychopathologies and suggest neurobiological models underlying these pathologies. The ultimate goal of this review is to stimulate new avenues of research that have direct links to molecular biology, and thus could prove to be invaluable to progress in the understanding and treatment of psychiatric disabilities.

Animals↗

Sodium deficiency and salt appetite in ICR: CD1 mice.

Using an outbred strain of mouse, we examined several characteristics of sodium appetite induced by depletion. We found that an appetite for 0.15 M NaCl solution was stimulated 24 h after injection of furosemide and access to a low-sodium diet, but not by low-sodium diet alone. When the duration of exposure to low-sodium diet was increased from 1 to 7 days, there was no additional effect on either the appetite or the blood plasma changes including elevated hematocrit ratio, protein and aldosterone concentrations, and plasma renin activity (PRA). Mice also showed an appetite for hypertonic (0.5 M) NaCl in solutions or in a gel matrix; the intakes of these two were comparable but the gel measurement was gravimetric so maybe more accurate. In the same study, we showed that single injections of either 10 or 40 mg/kg furosemide followed by a 24-h low-sodium diet produced similar appetites, but that 2.5 mg/kg had a submaximal effect. Lastly, we further validated the use of the gel matrix by showing in chronically depleted mice that intake was inversely related to NaCl concentration in the range 0.5-1.5 M, and that appetite was selective for sodium but not the anion with which it was paired.

Analysis of Variance↗

Dissociation of the effects of preload volume and energy content on subjective appetite and food intake.

Previous research suggests that enhancing the volume of a food preload without altering energy content can result in reduced appetite, although the limited evidence means that the conditions under which this effect will occur are not yet clear. In the present study, we used a Universal Eating Monitor (UEM) to record test meal intake constantly, in parallel with appetite ratings, following soup-based preloads that varied both in volume (150 vs. 450 ml) and energy density (1.4 vs. 4.2 kJ/ml). Healthy young men (n=20) received four different preload conditions (repeated measures) followed by unlimited hot pasta test meals (interval 30 min). They completed appetite ratings during and after each laboratory session, and food diaries for the afternoon and evening following each session. Subjective appetite after the preloads was reduced by the high-volume preloads relative to low-volume preloads, with no difference between the two at each volume level. This indicates an effect of volume, but no effect of energy. Test meal intake in the high-volume, high-energy-density condition was reduced relative to the other conditions, which did not differ from one another. This indicates an effect of total energy, but no effect of volume. The dissociation between these different measures of appetite might be explained in terms of largely cognitive influences on subjective appetite between preload and test meal, contrasted with stronger physiological influences on actual intake during the test meal. With regard to previous studies, it is argued that food volume is more influential under circumstances where gastric volume is closer to its normal limits.

Adult↗

Effects of naltrexone on food intake and changes in subjective appetite during eating: evidence for opioid involvement in the appetizer effect.

The effects of 50 mg naltrexone on eating and subjective appetite were assessed in a double-blind placebo-controlled study with 20 male volunteers. Appetite was monitored using a disguised digital balance connected to a micro-computer, which constantly monitored the amount of food remaining, and which automatically interrupted feeding for 30 s after every 50 g consumed to allow appetite ratings to be made. Half the subjects ate pasta with a cheese sauce, and the remainder pasta with a tomato sauce. Subjects ate significantly less of both foods after 50 mg naltrexone than in either the placebo condition or on the initial (familiarisation) day. Naltrexone also reduced the rated pleasantness of both foods, and reduced overall eating rate. When best-fit quadratic functions were used to describe changes in rated hunger in relation to intake within the meal, naltrexone abolished the positive linear component reflecting the initial stimulation of appetite without altering either intercept or the negative quadratic function. Although mood ratings suggested that naltrexone had a mild sedative effect, mood changes alone could not explain the effects of naltrexone on appetite. Overall, these data suggest a specific role for opioids in the stimulation of appetite through palatability.

Adult↗

NaCl appetite in two strains of rat reported to be resistant to mineralocorticoid-induced hypertension.

Both Long-Evans (LE) and Wistar-Furth (WF) strains of rat are known to be resistant to development of hypertension by mineralocorticoid (MC) treatment. MC-induced hypertension is, in part, mediated by the brain. We have examined another aspect of central MC action, the induction of NaCl appetite in these strains, by using the more common Sprague-Dawley (SD) and Wistar (WS) strains for comparison. In the first experiment, LE and SD rats were administered three treatments known to induce an appetite for NaCl solution in rats. Administration of deoxycorticosterone acetate (DOCA) increased the intake of 0.45 M NaCl in both strains, but the amounts consumed were about 2-fold greater in LE rats than in SD rats. Administration of captopril also increased NaCl intake, but there were no differences between LE and SD rats. NaCl depletion with furosemide induced NaCl appetite in both strains, but the amounts consumed were about 2-fold greater in LE rats than in SD rats. In the second experiment, adult male WF and WS rats were administered DOCA, enalapril, or furosemide and NaCl appetite was determined. Both strains showed comparable NaCl appetite during each of these treatments. However, during a 5-week regimen of DOCA with only NaCl-KCl solution to drink, uninephrectomized WF rats consumed less than WS rats. Thus, despite reported resistance to MC-induced hypertension, neither LE nor WF strains of rats showed correspondingly marked deficits in induced NaCl appetite.

Analysis of Variance↗

Effects of dopamine agonists on appetitive and consummatory male sexual behavior in Japanese quail.

The effects of pharmacological manipulations of dopaminergic transmission on appetitive and consummatory aspects of male sexual behavior were investigated in castrated male Japanese quail treated with exogenous testosterone. Appetitive male sexual behavior was assessed by measuring a learned social proximity response and consummatory behavior was assessed by measuring copulatory behavior per se. The nonselective dopamine receptor agonist, apomorphine, inhibited in a dose-dependent manner both components of male sexual behavior. Two indirect dopamine agonists were also tested. Nomifensine, a dopamine re-uptake inhibitor, decreased appetitive sexual behavior but increased the frequency of mount attempts, a measure of consummatory sexual behavior. Amfonelic acid, a compound that enhances dopaminergic tone by a complex mechanism, increased aspects of both appetitive and consummatory behaviors. These data suggest that, in quail, as in rodents, increases in dopaminergic tone facilitate both appetitive and consummatory aspects of male sexual behavior. Apomorphine may be inhibitory in quail because it acts primarily on D2-like receptors, unlike in rats, where it stimulates sexual behavior and acts primarily on D1-like receptors at low doses but interacts with D2-like receptors at higher doses. This is supported by the observation that stereotyped pecking, a behavior stimulated selectively in quail by D2 agonists, was increased by apomorphine but not by the two indirect agonists. The observed partial dissociation between the effects of these dopaminergic agonists on appetitive and consummatory sexual behaviors suggests that these two components of male sexual behavior may be controlled by the action of dopamine through different neuronal systems.

Animals↗

Effects of brain testosterone implants on appetitive and consummatory components of male sexual behavior in Japanese quail.

Aromatization of testosterone (T) into an estrogen is necessary for the activation of consummatory and appetitive sexual behavior in male Japanese quail. T action within the medial preoptic nucleus (POM) is necessary and sufficient to activate consummatory behavior, and some evidence suggests that POM might be involved in the control of appetitive behavior, but other brain regions, such as the bed nucleus of the stria terminalis (BST), an area that contains a dense population of aromatase-immunoreactive neurons, are also likely to be involved. This study was performed to assess the effects of stereotaxic T implants targeting either the POM or the BST on the activation of both components of sexual behavior in castrated male quail. Appetitive sexual behavior was measured by an acquired social proximity response in which a male will approach a window providing visual access to a female after the window has been repeatedly paired with physical access to a female and the possibility to freely interact with her. Rhythmic cloacal sphincter movements that are produced by the male when given visual access to a female were used as another measure of appetitive sexual behavior that does not appear to depend on sexual learning. The experiments confirmed that copulation is necessary for males to develop the social proximity response that is used to measure the appetitive sexual behavior. T implants in the POM activated both components of sexual behavior, suggesting that these components cannot be completely dissociated. In contrast, T implants located within the BST did not affect either component, but because implants in the BST did not activate copulatory behavior, these results do not preclude a role for BST in the expression of a previously acquired appetitive sexual behavior.

Analysis of Variance↗

Thirst and sodium appetite after colloid treatment in rats with septal lesions.

Previous experiments in which angiotensin II (AII) and mineralocorticoids were administered to rats have suggested that these hormones play a natural role in mediating thirst and sodium appetite. This hypothesis was examined by making use of rats with septal lesions, which have an apparent sensitivity to the central effects of AII, and studying their behavioral response to subcutaneous colloid treatment, which produces hypovolemia and thereby stimulates the secretions of renin and aldosterone. The induced thirst and sodium appetite both were markedly enhanced in the brain-damaged animals. However, water intake was not increased when the hypovolemia was moderate, and sodium appetite was augmented only when animals had been sodium deprived, a procedure known to potentiate aldosterone secretion. These findings support previous suggestions that whereas AII normally contributes little to thirst, it may help to mediate sodium appetite in rats when aldosterone is abundant. Finally, the two drives were not elicited uniformly; those animals that drank the most water after colloid treatment consumed the least saline. These findings suggest that whereas septal lesions may sensitize the rat's brain to the sodium-appetite-eliciting effects of AII as well as to its dipsogenic effects, sodium appetite emerges only if the induced thirst is not too pronounced.

Aldosterone↗

Dependence of adrenalectomy-induced sodium appetite on the action of angiotensin II in the brain of the rat.

Adrenalectomized rats express a robust sodium appetite that is accompanied by high levels of blood-borne angiotensin II and is caused by angiotensin II of cerebral origin. Blood-borne angiotensin II is elevated in rats consuming NaCl after adrenalectomy, and plasma angiotensin II concentrations are increased further when the animals cannot drink a NaCl solution. These phenomena are the result of the pathological removal of aldosterone, because replacement therapy returned both sodium intake and plasma angiotensin II concentrations to preadrenalectomy levels. The adrenalectomized rat's appetite for sodium is completely suppressed by interference with the central, but not the peripheral, action of angiotensin II. These data demonstrate that the mechanism of the sodium appetite of the adrenalectomized rat is a pathological instance of the angiotensin/aldosterone synergy that governs the sodium appetite of the adrenal-intact, sodium-depleted rat. Because aldosterone has been removed, angiotensin acts alone to produce the appetite. Furthermore, the data show that it is angiotensin II of central origin that is important for sodium appetite expression.

Adrenal Glands↗

Preferential activation of midbrain dopamine neurons by appetitive rather than aversive stimuli.

Midbrain dopamine systems are crucially involved in motivational processes underlying the learning and execution of goal-directed behaviour. Dopamine neurons in monkeys are uniformly activated by unpredicted appetitive stimuli such as food and liquid rewards and conditioned, reward-predicting stimuli. By contrast, fully predicted stimuli are ineffective, and the omission of predicted reward depresses their activity. These characteristics follow associative-learning rules, suggesting that dopamine responses report an error in reward prediction. Accordingly, neural network models are efficiently trained using a dopamine-like reinforcement signal. However, it is unknown whether the responses to environmental stimuli concern specific motivational attributes or reflect more general stimulus salience. To resolve this, we have compared dopamine impulse responses to motivationally opposing appetitive and aversive stimuli. In contrast to appetitive events, primary and conditioned non-noxious aversive stimuli either failed to activate dopamine neurons or, in cases of close resemblance with appetitive stimuli, induced weaker responses than appetitive stimuli. Thus, dopamine neurons preferentially report environmental stimuli with appetitive rather than aversive motivational value.

Animals↗

Modulation of feeding-induced activation of mesolimbic dopamine transmission by appetitive stimuli and its relation to motivational state.

We have previously shown in non-deprived rats that feeding of an unfamiliar palatable food (Fonzies(R)) phasically stimulates in vivo dopamine (DA) transmission in the medial nucleus accumbens (NAc) and this effect undergoes habituation after a previous (24 h) Fonzies meal (Bassareo & Di Chiara 1997, J. Neurosci., 17, 851-861). The present study shows that an unfamiliar food (Kinder(R)) with a taste and composition (milk chocolate) different from that of Fonzies, also induces a release of DA in the NAc subjected to one-trial habituation. Habituation was taste specific as no cross-habituation was observed between Fonzies and Kinder. In undeprived rats, a 40-min exposure to an intrinsic appetitive stimulus (food smell arising from a Fonzies-filled plastic box) also prevented the increase in dialysate DA associated with Fonzies feeding, and this effect was partially reversed by food deprivation. Food deprivation also prevented habituation of Fonzies-induced increase of dialysate DA in the NAc. Predictive association of an empty plastic box to Fonzies feeding resulted in the acquisition of appetitive properties by the box and in facilitation (rather than inhibition) of the phasic responsiveness of DA transmission to Fonzies feeding. A 10-min pre-exposure to appetitive olfactory stimuli intrinsic to Fonzies still prevented, like a 40-min pre-exposure, the NAc DA response to Fonzies feeding; however, a 5-min pre-exposure to these appetitive stimuli did not prevent the DA response in the NAc. These results show that the phasic responsiveness of NAc DA transmission to an unfamiliar palatable food is under strong modulatory control by primary (consummatory) and secondary (appetitive) stimuli, and that the sign and extent of this control depends on the nature of the appetitive stimulus, delay of reward and motivational state (deprivation).

Animals↗

Appetite sensations as a marker of overall intake.

The aim of this study was to evaluate the clinical utility of appetite sensations to characterize individual overall energy intake. A group of men (n 28) and women (n 23) was recruited to record their 'desire to eat', 'hunger', 'fullness' and 'prospective food consumption' (PFC) on visual analogue scales before a standardized meal test, immediately after and every 10 min for a period of 1 h after the meal. The 1 h post-meal area under the curve (1 h AUC) and the satiety quotient (SQ) were calculated for all appetite sensations. In a second visit, all participants were invited to eat three meals in order to measure total energy intake (TEI) and food preferences. Metabolic rate (MR) was also assessed to derive daily relative energy intake (REI) by subtracting this variable from TEI (TEI-MR=REI). The Three-Factor Eating Questionnaire scores were also calculated for all participants. One h AUC for fullness was the appetite sensation most strongly associated with TEI and REI (r-0.42, P< or =0.003 and r-0.32, P< or =0.05, respectively). SQ for fullness was the only predictor of TEI and REI (r-0.42, P< or =0.0003 and r-0.30, P< or =0.05, respectively). Restraint, disinhibition and hunger scores were not associated with appetite sensation variables. These results suggest that the fullness dimension seems to be a useful appetite sensation to predict long-term TEI and REI. Thus, assessment of appetite sensation such as fullness in response to a fixed load may be useful to evaluate individual overall energy intake.

Adult↗

Interaction of insulin, glucagon-like peptide 1, gastric inhibitory polypeptide, and appetite in response to intraduodenal carbohydrate.

The relation between gastrointestinal incretin hormones in the control of insulin release and short-term satiety by intestinal carbohydrate was investigated in 8 fasted, healthy male volunteers. Insulin, gastric inhibitory polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and appetite ratings were measured during, and food intake was measured after, intraduodenal infusions of glucose or saline. Studies were conducted under hyperinsulinemic and euglycemic conditions. Raising plasma insulin with intravenous insulin infusion to concentrations slightly above usual postprandial concentrations (356.4 +/- 4.8 pmol/L) had no effect on GIP, GLP-1, or appetite ratings before the intraduodenal infusions began. Intraduodenal glucose infusion resulted in a further increase in plasma insulin to a peak of 779.4 +/- 114.0 pmol/L, caused an early increase in plasma GIP and a later increase in GLP-1 concentrations (P < 0.01), suppressed appetite (P < 0.05), and reduced energy intake (P < 0.01) compared with intraduodenal infusion of saline. There was a close association between the increase in GLP-1 and decrease in appetite. Infusion of octreotide to suppress the release of gastrointestinal hormones prevented the rise in insulin, GIP, and GLP-1 induced by intraduodenal glucose infusion and reversed the suppression of appetite and reduction in energy intake. These results suggest that 1) when infused to result in plasma concentrations slightly above usual postprandial concentrations, insulin does not inhibit its own release and 2) the effects of intraduodenal glucose on appetite may be mediated through the release of GLP-1 and not insulin.

Adult↗

Glycemic and insulinemic responses as determinants of appetite in humans.

BACKGROUND: The importance of the postprandial glycemic and insulinemic responses for appetite and energy intake (EI) is controversial. OBJECTIVE: The aim of the study was to test the hypothesis that postprandial appetite sensations and subsequent EI are determined by postprandial glycemic and insulinemic responses after the intake of a range of breakfast meals. DESIGN: The study was a randomized, crossover meal test including 28 healthy young men, each of whom tested 10 of 14 breakfast meals. Each meal contained 50 g carbohydrate with various glycemic index and energy and macronutrient contents. Blood samples were taken, and appetite sensations were measured 3 h after the meals. Subsequently, EI at lunch (EI(lunch)) was recorded. RESULTS: The glycemic response was unrelated to appetite sensations, whereas the insulinemic response was positively associated with postprandial fullness (R2 = 0.33, P < 0.05). In contrast, the insulinemic response was unrelated to the subsequent EI(lunch), whereas the glycemic response was positively associated with EI(lunch) (R2 = 0.33, P < 0.05). Although no significant difference in EI(lunch) was observed between different breakfast conditions, a low breakfast EI was associated with a high EI(lunch) (R2 = 0.60, P < 0.001). CONCLUSIONS: The current study does not support the contention that the postprandial glycemic response has an important effect on short-term appetite sensations, but a low-glycemic index meal may reduce subsequent EI. In contrast, postprandial insulin seems to affect short-term appetite sensations.

Adult↗

Full expression of the exaggerated salt appetite of the spontaneously hypertensive rat requires a prenatal factor.

1. The spontaneously hypertensive rat (SHR) exhibits a lower bodyweight in utero and an exaggerated salt appetite post partum. To determine whether salt appetite is affected by the perinatal environment, we measured the salt appetite of embryo-cross-transferred SHR and Wistar Kyoto (WKY) rats at maturity. 2. One-cell embryos were collected from the oviducts of donor rats and transferred into the oviducts of recipients through the infundibulum. The salt appetite of the resultant female offspring for 0.10 and 0.15 mol/L saline was measured at 20-30 weeks of age. 3. Salt intake of SHR gestated in WKY rats was significantly lower than that of SHR gestated in SHR, while that of WKY rats gestated in SHR was higher than that of WKY rats gestated in WKY rats. 4. Therefore, some maternal factor plays a role in the development of the exaggerated salt appetite of the SHR. This factor is also able to affect the later salt appetite of WKY rat offspring born to SHR surrogates.

Animals↗

The willingness to eat. An investigation of appetite among elderly people.

The aim of this study was to identify and describe factors of importance with regard to appetite among elderly people. A qualitative approach was used and the method was grounded theory. Fifteen elderly people were interviewed using a method with two overall questions. The results show that the willingness to eat plays a central role in appetite among elderly people. The appetite is a state on a sliding scale, from good to poor appetite. Factors affecting the appetite include six categories: mood, personal values, wholesomeness, food, eating environment and meal fellowship. When planning and realizing nursing actions concerning eating, the willingness to eat has to be observed. The desire within every individual has to be given consideration, including all factors as well as how they affect each other. The willingness to eat contains internal factors dependent on mood and personal values, as well as external factors dependent on wholesomeness, food, eating environment and meal fellowship. These factors contain qualitative dimensions, which affect elderly people's appetites as well as their quality of life to a varying extent. Through this, it can be seen that there is a connection between their desire or willingness to eat and their will to live.

Affect↗

Effect of brain serotoninergic stimulation on sodium appetite of euthyroid and hypothyroid rats.

The aim of the present work was to investigate the role of the serotoninergic system in the control of sodium appetite of hypothyroid rats (HTR) by administering drugs that affect the serotoninergic activity, and to compare the same homeostatic behaviour in euthyroid rats (ETR) also given these drugs. Fenfluramine (FEN; 5.0 mg x kg(-1), I.P.), which releases serotonin in the brain, significantly reduced the intake of 1.8 % NaCl in HTR subjected to water and sodium depletion (depleted) or water, sodium and food deprivation (deprived) by 31 and 45 %, respectively, 120 min after FEN injection, compared to HTR that received vehicle alone. Similarly, administration of FEN to ETR reduced 1.8 % NaCl intake in depleted and deprived rats by 64 and 46 %, respectively. The presynaptic serotonin reuptake inhibitor fluoxetine (20.0 mg x kg(-1), I.P.) led to the inhibition of sodium appetite in HTR during the initial 30 min in depleted rats and for up to 60 min post-injection in deprived rats, while sodium appetite inhibition persisted for longer periods in ETR. The 5HT2C receptor agonist mCPP (5.0 mg x kg(-1), I.P.) caused a drastic reduction in sodium appetite in HTR and ETR in depleted and deprived rats, respectively, after 120 min. Prior administration of the 5HT2C receptor antagonist LY53857 (5.0 mg x kg(-1), I.P.) completely blocked the inhibitory action of mCPP on sodium appetite in both HTR and ETR. In summary, our results suggest that the recruitment of serotoninergic neurons involved in the modulation of sodium appetite seems to be decreased in hypothyroidism due to a probable deficiency in the cerebral signalling pathway.

Animals↗