Methylphenidate is the first-choice treatment for attention-deficit/hyperactivity disorder (ADHD), but its mechanism of action is incompletely understood. The cognitive effects of methylphenidate have been extensively studied, but little is known about its effects on spontaneous social behavior. During adolescence, rats display a characteristic, highly vigorous form of social behavior, termed social play behavior, which is of critical importance for social and cognitive development. We investigated the neurobehavioral mechanisms by which methylphenidate affects social play behavior in rats. Methylphenidate (0.3-3.0 mg/kg, s.c. or p.o.) abolished social play behavior, without altering general social interest. This effect of methylphenidate did not depend upon the baseline level of social play and was not secondary to changes in locomotion. Furthermore, the play-suppressant effect of methylphenidate was not subject to tolerance or sensitization. Methylphenidate blocked both the initiation to play and the responsivity to play initiation. The effect of methylphenidate was mimicked by the noradrenaline reuptake inhibitor atomoxetine, which is also used for the treatment of ADHD, and was blocked by an a-2 adrenoceptor antagonist. In addition, combined administration of subeffective doses of methylphenidate and atomoxetine suppressed social play. However, blockade of a-1 adrenoceptors, b-adrenoceptors, or dopamine receptors did not alter the effect of methylphenidate. These data show that methylphenidate selectively blocks the most vigorous part of the behavioral repertoire of adolescent rats through a noradrenergic mechanism. We suggest that the effect of methylphenidate on social play is a reflection of its therapeutic effect in ADHD, that is, improved behavioral inhibition. However, given the importance of social play for development, these findings may also indicate an adverse side effect of methylphenidate.
Background: Protein is an indispensable component within the human diet. It is unclear, however, whether behavioral strategies exist to avoid shortages.Objective: The objective was to investigate the effect of a low protein status compared with a high protein status on food intake and food preferences.Design: We used a randomized crossover design that consisted of a 14-d fully controlled dietary intervention involving 37 subjects [mean ± SD age: 21 ± 2 y; BMI (in kg/m2): 21.9 ± 1.5] who consumed individualized, isoenergetic diets that were either low in protein [0.5 g protein · kg body weight (BW)−1 · d−1] or high in protein (2.0 g protein · kg BW−1 · d−1). The diets were followed by an ad libitum phase of 2.5 d, during which a large array of food items was available, and protein and energy intakes were measured.Results: We showed that in the ad libitum phase protein intake was 13% higher after the low-protein diet than after the high-protein diet (253 ± 70 compared with 225 ± 63 g, P < 0.001), whereas total energy intake was not different. The higher intake of protein was evident throughout the ad libitum phase of 2.5 d. In addition, after the low-protein diet, food preferences for savory high-protein foods were enhanced.Conclusions: After a protein deficit, food intake and food preferences show adaptive changes that suggest that compensatory mechanisms are induced to restore adequate protein status. This indicates that there are human behavioral strategies present to avoid protein shortage and that these involve selection of savory high-protein foods. This trial was registered with the Dutch Trial register at http://www.trialregister.nl as NTR2491.
Protein status modulates brain responses in reward regions to savory food cues. These novel findings suggest that dietary protein status affects taste category preferences, which could play an important role in the regulation of protein intake in humans. This trial was registered at www.trialregister.nl/trialreg/admin/rctview.asp?TC=3288 as NTR3288.
Taste is involved in food preference and choice, and it is thought that it can modulate appetite and food intake. The present study investigated the effect of savory or sweet taste on satiation, reward, and food intake and according to individual differences in eating behavior traits underlying susceptibility to overeating. In a crossover design, 30 women (BMI = 22.7 ± 2.3; age = 21.9 ± 2.6 y) consumed a fixed energy preload (360 kJ/g) with a savory, sweet, or bland taste before selecting and consuming items from a test meal ad libitum. Sensations of hunger were used to calculate the satiating efficiency of the preloads. A computerized task was used to examine effects on food reward (explicit liking and implicit wanting). The Three Factor Eating Questionnaire was used to compare individual differences in eating behavior traits. Satiation and total food intake did not differ according to preload taste, but there was an effect on explicit liking and food selection. The savory preload reduced liking and intake of high-fat savory foods compared to sweet or bland preloads. The eating behavior trait disinhibition interacted with preload taste to determine test meal intake. Higher scores were associated with increased food intake after the sweet preload compared to the savory preload. Independent of preload taste, disinhibition was associated with lower satiating efficiency of the preloads and enhanced implicit wanting for high-fat sweet food. Savory taste has a stronger modulating effect on food preference than sweet or bland taste and may help to preserve normal appetite regulation in people who are susceptible to overeating.
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