Food reward

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== Motivated behaviour and food as a reinforcer ==

The underlying pathways in motivating feeding behaviour seem to be far more complex than a simple homeostatic system, which responds to metabolic and satiety signals from the gut. One possible thought is that the brain’s reward systems react to stimuli such as sight, smell and taste, or other cues that predict food. However, neither hunger nor thirst results in unconditioned goal-directed behaviour. Chance encounters with various tastes of palatable foods are required before goal-directed behaviour can result from the interaction of the internal needs with the salience of environmental stimuli. For example an infant recognises and learn to seek out sweet tastants, but the desire for a particular food is controlled by the interaction of peptide levels (related to hunger) with the brain circuitry, coding the animal’s reinforcement history for that specific food. Subsequently, the infant will indiscriminately taste both food and non-food objects, until it has received reinforcing feedback from sufficient stimuli. In addition, the monkey’s appetite for a yellow banana requires the prior learning of the relation of the sight of the yellow skin of a banana, with the sweet taste of the white banana meat plus the consequences resulting from the ingestion of the fruit. Therefore, preference for a specific food, results only when the post-ingestional consequences of that food’ reinforce’ the tendency to eat that food. Thus, food is considered to be a strong reinforcer. Moreover, when the response of a behaviour stimulated by a reinforcer increases the rate of that specific behaviour; that is known as positive reinforcement or reward learning, and the positive events are called rewards. The reinforcing efficacy of food reward is the ability of the reward to maintain rather than to establish behaviour; consequently the stimulus learning contributes to the response learning. Dopamine is known to play an important role in both. However, evidence from various studies seem to conclude that dopamine’s contribution appears to be chiefly to cause ‘wanting’ (Dopamine signalling in the dorsal striatum/CPu) for hedonic rewards rather than ‘liking’ or learning (mesolimbic dopamine) for those rewards. The first evidence for the implication of dopamine in food reward came from studies in rats, where dopamine antagonists blocked the rewarding effects of brain stimulation (Liebman & Butcher 1974; Fouriezos & Wise 1976) and of psychomotor stimulants.

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You can also insert diagram. The role of the Mesolimbic Dopaminergic Reward System

Human eating behaviour is not solely dependent on the homeostatic measures controlled by the hypothalamus but also the dopaminergic system which is activated by various stimuli; auditory, visual, tactile, olfactory and gustatory. The dopaminergic system was first connected with the reward system (de Wit & Wise 1977) in response to pharmacological and genetic approaches. They clearly established that dopamine was involved in motivation, as a deficit results in the starvation and dehydration of the mouse which ultimately results in death. (Palmiter 2007) In the ‘reward circuit’, projections from the Ventral Tegmental Area (VTA) to the Nucleus Accumbens (NAc) have received the most attention due to the focus of studies on the hedonic impact from drugs and their possible roles in reinforcement, reward and addiction. These results have often led to the conclusion that dopamine action in the NAc is needed for motivation to acquire food or addictive drugs. Most reviews suggest that the projections from the VTA-NAc are needed for motivation to eat not consumption, this is due to lesion experiments which have shown that even when the VTA-NAc pathway has been destroyed the mice still manage to eat (Wise 2006). The Dopamine Hypothesis Dopamine signalling from the VTA to the NAc, hippocampus, amygdale and/or pre-frontal cortex promotes reward-related activities. Dopamine signalling in these brain regions focuses attention to salient environmental events and thereby facilitates behaviour towards directed goals. Also it is thought that dopamine released from the VTA also forms associations to promote learning between food reward and the environment (Palmiter 2007) However the role of mesolimbic dopamine seems to be controversial. Dopamines’ possible role in relation to reward? • Hedonia – Dopamine in the NAc acts as a pleasure neurotransmitter. Proposed due to drug activity. Not all rewards activate the reward system suggesting that the mesolimbic pathway is not solely hedonic. • Learning – predictions of future rewards, NAc and VTa lesions do not affect this part but lack the motivation for the reward. • Incentive Salience – the ‘wanting’ of the reward, released when there is a stimulus worth working hard for. In absence of DA the environmental stimulus go unnoticed and the animal eventually dies due to starvation and dehydration. The incentive salience theory seems to best fit the data in this field according to Berridge (2007). Therefore dopamine causes the wanting of the reward after the appropriate stimuli have been processed in the reward system. An elevation of dopaminergic transmission is needed to form these associations. It has been shown that an increase in extracellular dopamine is seen in regard to natural rewards, food, water and sex, during acute administration (Wise & Rompre 1989, Spanagel & Weiss 1999). However it must be noted that novelty is an important factor in the increased release from the NAc. It has been suggested by Palmiter, 2008 that the role of dopamine in motivation is split between the 2 dopaminergic pathways; the NAc and CPu pathways. The SNpc-CPu pathway is essential for motivation with dopamine signalling from the VTA-NAc needed in regard to modulating the actions of the other dopaminergic pathway.

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