Food is one of the primary stimuli essential for an organism survival, since it assures the necessary caloric resources to pursue physiological activities. As the other primary stimuli, food is endowed with rewarding properties fundamental to sustain the behaviors aimed at foraging, consuming and planning the appropriate strategy to repeat the pleasurable experience. In fact, the caloric content represents the primary value, but animals discriminate foods on the basis of their flavor and taste, and the taste-calorie association represents the incentive value of nutrients that influences subsequent food choices.
Many neuronal systems are involved in the complex regulation of the responses involved in food intake and energy homeostasis. In particular, a robust literature demonstrates an adaptive stimulation of dopamine transmission in response to food consumption preferentially in the nucleus accumbens shell (NAcS), a terminal area of the dopaminergic mesolimbic system, even in the absence of a caloric need provided that the food is highly palatable. Although the hedonic quality of a food is independent of dopaminergic transmission, the phasic increase in mesolimbic dopamine trasmission induced by palatable food consumption confers to it motivational value and salience. The pleasurable perception induced by palatable food is primarily mediated by ?-opiod and endocannabinoid receptors stimulation. The role played by ?-opiod receptors stimulation in specific subcortical areas (particularly, the NAcS, the central nucleus of the amygdala, and the ventral pallidum) in enhancing taste hedonics and driving food intake is well established. Furthermore, other neuronal systems, for example the orexinergic and cannabinoid systems, several hormones (ghrelin, leptin, amylin, insulin) and neuropeptide Y are implicated in the modulation of the rewarding and/or incentive properties of food.
The complex integration of peripheral signals and central effector systems results in the behavioral and physiological outputs that regulate food intake and energy expenditure. One consequence is that the drive to eat decreases when food is ingested. However, the motivation to eat or stop eating is more complex than the straightforward response to a homeostatic system. In fact, the brain reward systems when stimulated by the sight, smell and taste of food may override the homeostatic system and promote food consumption that exceeds caloric needs. Thus, palatability is a crucial factor in guiding the choice and the amount of food consumed.
In eating disorders, the function of the neuronal systems involved in the control of food intake and energy homeostasis and their interplay are likely altered and, in particular, it has been proposed that a loss of adaptive regulation of food-stimulated increase in dopamine transmission in the NAcS may play a relevant role in these disorders.
This Research Topic will be aimed at providing an up-to-date analysis of some relevant central mechanisms involved in the control of food responsiveness and intake, and the possible role played by the interaction between different neuronal systems. Moreover, this Topic will outline some of the modifications in these mechanisms that are hypothesized to underpin eating disorders characterized by compulsive food consumption, such as binge eating and bulimia nervosa.
Food is one of the primary stimuli essential for an organism survival, since it assures the necessary caloric resources to pursue physiological activities. As the other primary stimuli, food is endowed with rewarding properties fundamental to sustain the behaviors aimed at foraging, consuming and planning the appropriate strategy to repeat the pleasurable experience. In fact, the caloric content represents the primary value, but animals discriminate foods on the basis of their flavor and taste, and the taste-calorie association represents the incentive value of nutrients that influences subsequent food choices.
Many neuronal systems are involved in the complex regulation of the responses involved in food intake and energy homeostasis. In particular, a robust literature demonstrates an adaptive stimulation of dopamine transmission in response to food consumption preferentially in the nucleus accumbens shell (NAcS), a terminal area of the dopaminergic mesolimbic system, even in the absence of a caloric need provided that the food is highly palatable. Although the hedonic quality of a food is independent of dopaminergic transmission, the phasic increase in mesolimbic dopamine trasmission induced by palatable food consumption confers to it motivational value and salience. The pleasurable perception induced by palatable food is primarily mediated by ?-opiod and endocannabinoid receptors stimulation. The role played by ?-opiod receptors stimulation in specific subcortical areas (particularly, the NAcS, the central nucleus of the amygdala, and the ventral pallidum) in enhancing taste hedonics and driving food intake is well established. Furthermore, other neuronal systems, for example the orexinergic and cannabinoid systems, several hormones (ghrelin, leptin, amylin, insulin) and neuropeptide Y are implicated in the modulation of the rewarding and/or incentive properties of food.
The complex integration of peripheral signals and central effector systems results in the behavioral and physiological outputs that regulate food intake and energy expenditure. One consequence is that the drive to eat decreases when food is ingested. However, the motivation to eat or stop eating is more complex than the straightforward response to a homeostatic system. In fact, the brain reward systems when stimulated by the sight, smell and taste of food may override the homeostatic system and promote food consumption that exceeds caloric needs. Thus, palatability is a crucial factor in guiding the choice and the amount of food consumed.
In eating disorders, the function of the neuronal systems involved in the control of food intake and energy homeostasis and their interplay are likely altered and, in particular, it has been proposed that a loss of adaptive regulation of food-stimulated increase in dopamine transmission in the NAcS may play a relevant role in these disorders.
This Research Topic will be aimed at providing an up-to-date analysis of some relevant central mechanisms involved in the control of food responsiveness and intake, and the possible role played by the interaction between different neuronal systems. Moreover, this Topic will outline some of the modifications in these mechanisms that are hypothesized to underpin eating disorders characterized by compulsive food consumption, such as binge eating and bulimia nervosa.
