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{{CZ:(U00984) Appetite and Obesity, University of Edinburgh 2009/EZnotice}}
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A physiological response to ingestion of palatable food, resulting in behaviours directed towards eating.
Food intake involves both 'homeostatic feeding' (energy demands) and ‘non-homeostatic feeding’; the latter is associated with  '''food reward''', which involves both 'liking’ (pleasure/palatability) and ‘wanting’ (incentive motivation) according to the ''salience theory''. Experiments in mice suggest that ‘liking’ involves the release of mu-[[opioid peptide]]s in brain, while ‘wanting’ involves the neurotransmitter [[dopamine]] <ref>Berridge KC (2007) The debate over dopamine’s role in reward: the case for incentive salience. ''Psychopharmacology'' 191:391–431</ref>.  




 
{{Image|food intake diagram.jpg|right|400px|}}
=== '''Introduction''' ===
 
'''
Food intake is driven by both 'homeostatic feeding' (energy demands) and ‘non-homeostatic feeding’ (pleasure associated eating or preferred food). The latter is associated with the food reward processes, which is further categorized to’ liking’ (pleasure/palatability) and ‘wanting’ (incentive motivation) according to the Salience theory (Berridge K.C, 2007). Moreover, the salience model describes different brain mechanisms associated with each of the two components. Experiments using mouse models showed that the brain mechanisms attributed to ‘liking’ involve the neurotransmission of mu-opioids in the nucleus accumbens, ventral pallidum, parabrachial nucleus, and nucleus of the solitary tract, while mechanisms attributed to ‘wanting’ implicated the neurotransmitter dopamine secreted in brain areas such as the prefrontal cortex (PFC), amygdala, hypothalamus, and projections from the ventral tegmental area (VTA) to the nucleus accumbens (NAc)(Berridge K.C, 2007). Dopamine has an important role in both energizing and also reinforcing feeding. The focus of this article is the reinforcement of feeding, which is the primary role of [[dopamine]] and its involvement in food reward pathways. In addition, the action of dopamine in the dopaminergic systems and the interaction of this system with other reward systems is described. Finally the effect of other hormones such as [[insulin]], [[ghrelin]], and [[leptin]], on food reward is studied through their association with dopamine. The final part of this article links the aforementioned processes, particularly the dopaminergic pathway, with obesity. A description of what can go wrong, changes in the distribution of dopamine receptors, and a genetic approach is given, linking the function of the dopaminergic system and obesity by a gene, related in the reinforcing properties of food behaviour.
{{Image|food intake diagram.jpg|right|250px|Image Caption}}
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| '''Reinforcement''' - The process by which a stimulus strengthens a behavioural response so that the probability of response is increased when the stimulus is presented again.  
| '''Reinforcement''' - The process by which a stimulus strengthens a behavioural response so that the probability of response is increased when the stimulus is presented again.  
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==='''Motivated behaviour and food as a reinforcer'''===
==='''Motivated behaviour and food as a reinforcer'''===
The brain’s reward systems react to stimuli such as sight, smell and taste, and other cues that predict food. However, hunger cannot result in unconditioned goal-directed behaviour; <ref>Changizi MA ''et al.'' (2002) Evidence that appetitive responses for dehydration and food-deprivation are learned ''Physiol Behav'' 75:295–304</ref> chance encounters with palatable foods are required before goal-directed behaviour can occur, which link the internal needs with the salience of environmental stimuli <ref>Wise RA (2006) Role of brain dopamine in food reward and reinforcement ''Phil Trans R Soc Lond B Biol Sci'' 361:1149–58</ref>For exa mple, an infant recognises and learns to seek out sweet tastes, but the desire for any particular food is controlled by the interaction of peptide levels (related to hunger) with neural circuits in the brain which store the animal’s past experience of that particular food. <ref>Steiner JE ''et al.''(2001) Comparative expression of hedonic impact: affective reactions to taste by human infants and other primates ''Neurosci Biobehav Rev'' 25:53–74</ref> Subsequently, the infant will taste both food and non-food objects indiscriminately until it has received reinforcing feedback from enough stimuli. A monkey’s appetite for yellow bananas requires that the monkey learns to relate the sight of the yellow skin of a banana with the sweet taste of the banana, plus the consequences of eating it. Preference for a particular food results only when the post-ingestional consequences of that food ’reinforce’ the tendency to eat that food. For these reasons, food is considered to be a strong reinforcer. When the response of a behaviour stimulated by a reinforcer increases the frequency of that  behaviour; that is ''positive reinforcement'' or ''reward learning'', and the positive events are called ''rewards'' <ref>Epstein LH ''et al.''(2007) Food reinforcement and eating: a multilevel analysis ''Psychol Bull'' 133:884–906</ref>. 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.


The underlying pathways in motivating feeding behaviour seem to be far more complex than a simple homeostatic system, responding 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 (Wise, 2006). However, hunger can not result in unconditioned goal-directed behaviour (Changizi et al. 2002). Chance encounters with various palatable foods are required before goal-directed behaviour can occur, which links the internal needs with the salience of environmental stimuli (Wise, 2006).


For example, an infant recognises (Steiner et al. 2001) and learns to seek out (Johanson & Hall 1979)sweet tastants, but the desire for a particular food is controlled by the interaction of peptide levels with the brain circuitry. Where the peptide levels are related to hunger, and 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 (Wise, 2006). 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 (Wise, 2004b) 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. For the above reasons, 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 (Epstein, 2007). 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.
== Food reward pathways ==
 
{{Image|Dopamine pathway.jpg|right|500px|Mesolimbic Dopaminergic Reward System}}
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.


== Food reward pathways ==
The first evidence for the involvement of dopamine in food reward came from studies in rats, in which dopamine antagonists blocked the rewarding effects of brain stimulation and of psychomotor stimulants<ref>Liebman JM, Butcher LL (1974) Comparative involvement of dopamine and noradrenaline in rate-free self-stimulation in substantia nigra, lateral hypothalamus, and mesencephalic central gray ''N-S Arch Pharmacol''</ref> <ref>Fouriezos G, Wise RA (1976) Pimozide-induced extinction of intracranial self-stimulation: response patterns rule out motor or performance deficits ''Brain Res'' 103:377–80</ref>.
{{Image|Dopamine pathway.jpg|right|250px|Image Caption}}


==='''The role of the Mesolimbic Dopaminergic Reward System'''===


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 the motivation to eat but not for the food consumption. Lesion experiments have shown that even when the VTA-NAc pathway has been destroyed the mice still manage to eat. [[#References|(Palmiter R, 2007)]]
==='''The Mesolimbic Dopaminergic Reward System'''===
In the ‘reward circuit’, projections from the [[ventral tegmental area]] (VTA) to the [[nucleus accumbens]] have received the most attention. Dopamine action in the nucleus accumbens is thought to be needed for motivation to acquire food or addictive drugs. Most reviews suggest that the projections from the VTA to the nucleus accumbens are needed for the motivation to eat, but not for food consumption itself.  


'''The Dopamine Hypothesis'''<br />
'''The Dopamine Hypothesis'''<br />
Dopamine signalling from the VTA to the nucleus accumbens, [[hippocampus]], [[amygdala]] and/or pre-frontal cortex promotes reward-related activities. Dopamine signalling in these brain regions focuses attention to salient environmental events and facilitates behaviour towards directed goals. It is thought that dopamine released from the VTA also promotes learning between food reward and the environment.


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)<br />
'''Dopamine's role in reward?'''<br />
 
•''[[Hedonia]]'' – Dopamine in the nucleus accumbens has been said to act as a "pleasure" neurotransmitter. Not all rewards activate the reward system, suggesting that the mesolimbic pathway is not solely hedonic.
However the role of mesolimbic dopamine seems to be controversial. Dopamines’ (DA) possible role in relation to reward?<br />
 
• 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.<br />
 
• Learning – predictions of future rewards, NAc and VTa lesions do not affect this part but lack the motivation for the reward.<br />
 
• Incentive Salience – the ‘wanting’ of the reward, released when there is a stimulus worth working hard for. In absence of DA the environmental stimulus goes unnoticed and the animal eventually dies due to starvation and dehydration. <br />
 
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.<br />
 
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( see diagram). 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.
 
==='''The substantia nigra pars compacta (SNpc) to the caudate putamen (CPu): A critical dopaminergic pathway''' ===
It has been stated that the midbrain dopamine (DA) neurons are the key neural components for reward mechanisms (Satoh, T. et al (2003)). Creation and observation of dopamine deficient (DD) mice implied that DD mice starve because they are not motivated to respond to hunger signals (Palmiter, RD. (2008)). Thus, its been proposed that DA is crucial for mice to engage in the majority of goal-directed or motivated behaviours (Palmiter, RD. (2008)).
 
However in the literature there is much controversy as to the pathway used; a universal finding is the involvement of the striatum, the input structure of the basal ganglia in a circuit responsible for mediating goal-directed behaviour, with the striatum’s central role being the processing of reward like stimuli (Delgado, MR. (2007)).
The two proposed pathways are from the ventral tegmental area (VTA) to nucleus accumbens (NAc) (ventral striatum); or the substantia nigra pars compacta (SNpc) to the caudate putamen (CPu) (dorsal striatum) (Palmiter, RD. (2008)).
 
The striatum includes not only the dorsal region, which encompasses the caudate nucleus and putamen, but also the ventral region that includes the core and shell of the nucleus accumbens, see figure 2 (Wickens, JR. et al (2007)).


The bulk of reward information processing comes from animal models in the literature (Delgado, MR. (2007)).
•''Learning'' – predictions of future rewards, nucleus accumbens and VTA lesions do not affect this part but lack the [[motivation]] for the reward.
One study using nonhuman primates found that striatal neurons responded to the anticipation and delivery of reward (Delgado, MR. (2007)). Another study found reward-related dopamine response specifically in the mouse dorsal striatum, correlated with the delivery of food reward (Natori, S. et al. (2009)).  
•''[[Incentive Salience]]'' – the ‘wanting’ of the reward, released when there is a stimulus worth working hard for. In absence of dopamine, the environmental stimulus goes unnoticed and the animal will eventually die from starvation and dehydration.
The importance of the DA system in the dorsal striatum is demonstrated in a study using DD mice whose DA signalling is restored by viral rescue (Palmiter, RD. (2008), Darvas, M. & Palmiter, RD.(2009)) . These mice learned to lever press for food rewards as quickly as control mice and their motivation to work for food was restored (Darvas, M. & Palmiter, RD.(2009)). An important finding was that in DD deficient mice feeding was never restored after viral transduction in the NAc (Palmiter, RD. (2008)).


Recently, the advancement of neuroimaging techniques has allowed researchers to extend such investigations to the human brain (Delgado, MR. (2007)).
The incentive salience theory seems to best fit the data in this field. Therefore dopamine causes the wanting of the reward after the appropriate stimuli have been processed in the reward system. Dopamine transmission is needed to form these associations. An increase in extracellular dopamine is seen in regard to natural rewards, food, water and sex, during acute administration. However novelty is an important factor in the increased release from the nucleus accumbens. It has been suggested  that the role of dopamine in motivation is shared between the nucleus accumbens and CPu pathways(see diagram). The SNpc-CPu pathway is essential for motivation, while dopamine signalling from the VTA to the nucleus accumbens needed in regard to modulating the actions of the other dopamine pathway.
DA release increases in dorsal striatum of hungry participants when stimulated with food items, demonstrating its involvement in reward processing (Delgado, MR. (2007)). During the delivery of rewards fMRI signals were higher in the dorsal striatum, particularly the head of the CPu (Delgado, MR. (2007)).  
These findings strongly suggest the human dorsal striatums involvement in reward processing; with the CPu being an integral structure of a circuit involved in learning and updating current rewards with the aim of maximizing reward consumption (Delgado, MR. (2007)).


The role of DA signalling in the CPu cannot be ignored as viral restoration rescued feeding, whereas in the NAc it did not. It has been proposed that dopamine signaling in the CPu is essential for motivation while dopamine signaling in the NAc modulates this motivation and evaluation of reward like stimuli, see figure 2 (Palmiter, RD. (2008)).
==='''The substantia nigra pars compacta to the caudate putamen===
Dopamine-deficient mice starve, apparently because they are not motivated to respond to hunger signals. Thus, it has been proposed that dopamine is crucial for mice to engage in most goal-directed or motivated behaviours. However it is not clear ''which'' dopamine pathway is involved; a universal finding is the involvement of the striatum, the input structure of the basal ganglia in a circuit responsible for mediating goal-directed behaviour, with the striatum’s central role being the processing of reward like stimuli. The two proposed pathways are from the VTA to nucleus accumbens (ventral striatum); or the [[substantia nigra]] pars compacta to the [[caudate putamen]] (dorsal striatum). The striatum includes not only the dorsal region, which encompasses the caudate nucleus and [[putamen]], but also the ventral region that includes the core and shell of the nucleus accumbens<ref>Wickens JR ''et al.'' (2007) Striatal contributions to reward and decision making ''Ann NY Acad Sci'' 1104:192–212</ref>


==='''The effect of hormones on the dopaminergic reward system'''===
Our understanding of how reward information is processed comes mainly from studies in animal models. One study, using nonhuman primates, found that striatal neurons responded to the anticipation and delivery of reward <ref>Delgado MR (2007) Reward-related responses in the human striatum ''Ann NY Acad Sci'' 1104: 70–88</ref>  Another found a reward-related dopamine response specifically in the mouse dorsal striatum, correlated with the delivery of food reward  <ref>Natori S ''et al.'' (2009) Subsecond reward-related dopamine release in the mouse dorsal striatum ''Neurosci Res'' 63:267–72</ref>
The importance of dopamine in the dorsal striatum was demonstrated using dopamine-deficient mice whose dopamine signalling is restored by viral rescue. These mice learned to lever press for food rewards as quickly as control mice, and their motivation to work for food was restored. Importantly, in these dopamine-deficient mice, feeding was never restored after viral transduction in the nucleus accumbens.<ref>Darvas M, Palmiter RD (2009) Restriction of dopamine signaling to the dorsolateral striatum is sufficient for many cognitive behaviours ''PNAS'' 106;34:14664–9</ref><ref>Palmiter RD(2008) Dopamine signaling in the dorsal striatum is essential for motivated behaviors: lessons from dopamine-deficient mice ''Ann N Y Acad Sci'' 1129:35–46</ref>


The role of hormones such as [[Leptin]], [[ghrelin]] and [[insulin]] in the homeostatic control of energy balance has been extensively studied. These hormones reflect the size of energy stores, such as [[adipose tissue]], and feed into the medial hypothalamus to influence feeding behaviours and regulate food intake and energy expenditure in response to metabolic demand <ref> Magni P. et al. (2009) Feeding behavior in mammals including humans. Ann.N.Y.Acad.Sci. 1163:221-232. PMID 19456343</ref>. Recent evidence also implicates a role for such hormones in dopamine reward pathways <ref> Palmiter R.D (2007)Is dopamine a physiologically relevant mediator of feeding behaviour? TINS 30. 8:375-381  </ref>.  
Recent advances in [[neuroimaging]] has allowed researchers to extend such investigations to the human brain. Dopamine is released in the dorsal striatum of hungry participants when stimulated with food items. During the delivery of rewards, [[fMRI]] signals were higher in the dorsal striatum, particularly the head of the caudate putamen[[#References|(Delgado MR (2007))]]. It has been proposed that dopamine signaling in the caudate putamen is essential for motivation, while dopamine signaling in the nucleus accumbens modulates this motivation and evaluation of reward-like stimuli.


, [[#References|(Figlewicz DP, Benoit SC, 2009)]].   
==='''The effect of hormones on the dopamine reward system'''===
Plasma concentrations of [[ghrelin]], [[leptin]] and [[insulin]] reflect the size of energy stores, such as [[adipose tissue]], and act at the mediobasal [[hypothalamus]] to influence [[appetite]] and energy expenditure. These hormones also affect the dopamine reward pathways <ref>Figlewicz DP, Benoit SC (2009) Insulin, leptin, and food reward: update 2008 ''Am J Physiol'' 296:R9-19</ref> Receptors for these hormones are located on dopamine neurones in the VTA, and ligand binding results in activation e.g. by ghrelin <ref>Abizaid A ''et al.'' (2006) Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurones while promoting appetite ''J Clin Invest'' 116:3229–39</ref>
or inhibition e.g. by insulin or leptin of dopamine signalling to the nucleus accumbens <ref>Magni P ''et al.'' (2009) Feeding behavior in mammals including humans. ''Ann NY Acad Sci'' 1163:221-32</ref>.  These alterations in dopamine signalling pathways have complex effects on eating behaviours.   


Receptors for these hormones are located on dopaminergic neurones in the ventral tegmental area (VTA) [[#References|(Magni P. et al, 2009)]], and ligand binding results in activation e.g. by ghrelin [[#References|(Abizaid, A. et al, 2006)]], or inhibition e.g. by insulin or leptin of dopamine signalling to the nucleus accumbens (NAc) [[#References|(Magni P. et al, 2009)]].  These alterations in dopamine signalling pathways have complex effects on eating behaviours.  Many studies have reinforced the hypothesis that insulin and leptin attenuate the food reward, reducing incentive to eat [[#References|(Figlewicz DP, Benoit SC, 2009)]]. For example, behavioural studies showed that administering insulin or leptin to rats affected conditional place preference (CPP), which assesses the ability to relate a particular food reward to a particular environment [[#References|(Figlewicz DP, 2003)]]. Rats were fed a high fat diet and underwent a ‘training period’ prior to the test involving intracerebroventricular administration of insulin or leptin.  CPP was only abolished in those rats that received insulin or leptin treatment before or during the test as well as in training, whilst those who only received it in training maintained a normal CPP [[#References|(Figlewicz, D.P. et al, 2004)]].  This suggests that insulin and leptin influence the retrieval of food reward associations rather than the initial formation of these associations [[#References|(Figlewicz, D.P. et al, 2004)]]; presumably as a consequence of their inhibition of dopamine reward pathways.  These results have been reinforced by studies which have shown decreased sucrose self-administration in response to insulin or leptin administration [[#References|(Figlewicz DP et al, 2006]]) and decreased sucrose licking following insulin treatment [[#References|(Sipols AJ et al, 2000)]].  It is apparent that the high levels of insulin and leptin associated with obesity impair dopamine food reward pathways resulting in abnormal eating behaviours [[#References|(Figlewicz DP, Benoit SC, 2009)]].
Both insulin and leptin attenuate food reward, reducing the incentive to eat. For example, administering insulin or leptin to rats affected [[conditional place preference]] (CPP), which assesses the ability to relate a particular food reward to a particular environment. Rats were fed a high-fat diet and underwent a ‘training period’ before the test involving intracerebroventricular administration of insulin or leptin.  CPP was abolished in those rats that received insulin or leptin before or during the test as well as in training, whilst those who only received it in training maintained a normal CPP.  This suggests that insulin and leptin influence the ''retrieval'' of food reward associations rather than the initial formation of these associations.  These results have been reinforced by studies which have shown decreased sucrose self-administration in response to insulin or leptin, and decreased sucrose licking following insulin.<ref>Sipols AJ ''et al.'' (2000) Insulin and raclopride combine to decrease short-term intake of sucrose solutions.  ''Peptides'' 21:1361–7</ref> The high circulating concentrations of insulin and leptin associated with obesity impair dopamine food reward pathways resulting in abnormal eating behaviours.
 
''Table 1: Summary of effects of centrally administered insulin and leptin on reward behaviours''
'''Summary of effects of centrally administered insulin and leptin on reward behaviours'''
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*Adapted from [[#References|(Figlewicz, D.P. et al, 2004)]]  
*Adapted from Figlewicz ''et al.'' (2004)   


Ghrelin has been shown to increase dopamine signalling via ghrelin receptors on VTA neurones, via direct activation and also indirect manipulation of inputs onto the VTA to those of an excitatory nature [[#References|(Abizaid, A. et al, 2006)]].  However, it remains unclear whether this is a significant part the mechanism by which ghrelin stimulates feeding [[#References|(Palmiter R, 2007)]].
[[Ghrelin]] can increase dopamine signalling on VTA neurones, via direct activation and also indirect manipulation of inputs onto the VTA to those of an excitatory nature.  However, it is not clear whether this is a major part of the mechanism by which ghrelin stimulates feeding.<ref>Palmiter RD (2007) Is dopamine a physiologically relevant mediator of feeding behaviour? ''TINS'' 8:375-81</ref>
 
 
A major difficulty in elucidating the specific roles of these hormones in reward systems, and in general regulation of body weight, is that, due to the involvement of multiple hormones, manipulation of one results in activation of compensatory mechanisms, masking the physiological role of the manipulated hormone [[#References|(Palmiter R, 2007)]].  Furthermore, by manipulating levels of these hormones to abnormal levels, we can suggest potential functions for them, but this may not be relevant when they are found at physiological concentrations [[#References|(Palmiter R, 2007)]].  It should also be noted that the VTA possesses other neurons such as GABA-projection neurons, which also express receptors for the discussed hormones.  Therefore, we can not assume that these hormones affect feeding behaviours solely by their action on dopamine reward pathways.  It is also unclear whether these hormones act directly on dopamine reward pathways; insulin and leptin may influence dopamine reward systems by altering the activity of secondary peptide effector pathways, such as orexin A and melanocortins  [[#References|(Figlewicz DP, Benoit SC, 2009)]]. 
 
Much work, therefore, remains to be done to decipher the significance of results from these studies and the specific roles of hormones in food reward pathways [[#References|(Palmiter R, 2007)]].


==='''Opioid and cannabinoid systems'''===
==='''Opioid and cannabinoid systems'''===
Other reward systems, including the [[endogenous opioid]] and [[endocannabinoid]] systems interact with dopamine reward pathways.  Opioid peptides act in the nucleus accumbens to increase ‘wanting’ and ‘liking’ of food rewards. <ref>Pecina S (2008) Opioid reward 'liking' and 'wanting' in the nucleus accumbens  ''Physiol Behav'' 94:675-80</ref>Opioids also influence mesolimibic dopamine pathways by inhibiting GABAergic input onto the dopamine neurones of the VTA, resulting in increased dopamine release <ref>Spanagel R, Weiss F (1999) The dopamine hypothesis of reward: past and current status ''TINS'' 22:521-7</ref>.  The [[endocannabinoid]] system has also been implicated in reward behaviours, and cannabinoid receptors are expressed in several brain areas implicated in reward, including in the mesolimibic system.  Endocannabinoids modulate neurotransmission, and, for example, cannabinoid agonists stimulate dopamine release. Conversly, antagonising these receptors inhibits activation of dopamine release. <ref>Solinas M (2008) The endocannabinoid system in brain reward processes ''Br J Pharmacol'' 154:369-83</ref>


 
== Food reward and obesity ==
Other reward systems, including the endogenous opiate and [[endocannabinoid]] systems, also play a role in reward behaviours and interact with dopamine reward pathways [[#References|(Palmiter R, 2007)]].  Opiates act in the nucleus accumbens to increase ‘wanting’ and ‘liking’ of food rewards (Pecina S, 2008). Opioids also influence mesolimibic dopamine pathways by inhibiting GABAnergic input onto dopamine neurones on the VTA, resulting in increased dopamine release [[#References|(Spanagel and Weiss, 1999)]].  The [[endocannabinoid]] system has also been implicated in reward behaviours.  [[Endocannabinoids]] act to modulate neurotransmission in several brain areas; and they modulate dopaminergic transmission by inhibiting both excitatory and inhibitory input onto dopamine neurones [[#References|(Maldonado, R et al 2006)]].
There is a difference in dopamine activity between obese women and lean women/men in response to food and satiety. The obese have a higher metabolic activity in the parietal somatosensory area of the cortex which is linked to the sensory mouth, lips and tongue. Deficiencies of the dopamine D2 receptor may increase the likelihood of being obese. <ref>Wang ''et al.'' (2001) Brain dopamine and obesity. ''Lancet'' 357354-57</ref>  Obese people have fewer D2 receptors in the striatum and with both the D1 and D2 receptors acting synergistically to decrease feeding, this altered expression causes increased eating. The DRD2 gene is responsible for the reinforcing properties of food/addictive behaviour. <ref>Noble EP ''et al.''(1994) D2 dopamine receptor gene and obesity. ''Int J Eating Disorders'' 15:205–17</ref> Those who have the allelic variant A1 in this gene have fewer D2 receptors, making the dopamine reward circuits less sensitive.
 
== Food reward and Obesity ==
 
 
 
==='''The relationship between obesity and the dopaminergic system'''===
 
There is a difference in dopaminergic activity between obese women in comparison to lean women/men in response to food and satiety. It has been shown that the obese have a higher metabolic activity in the parietal somatosensory area of the cortex which is linked to the sensory mouth, lips and tongue. An increased amount of sensory processing in this brain region could increase the reinforcing properties of food (Epstein 2007).
 
Deficiencies of the D2 receptor have been suggested to increase the likelihood of being obese. Wang et al (2001) showed that obese people have fewer D2 receptors in the striatum and with both the D1 and D2 receptors acting synergistically to decrease feeding, this altered expression causes an increased amount of eating. The DRD2 gene is responsible for the reinforcing properties of food/addictive behaviour ( Noble 2003). Those who have the allelic variant A1 in this gene have fewer D2 receptors and therefore a decreased amount of dopamine signalling within the brain. This has been shown to be higher in obese individuals making the dopamine reward circuits less sensitive. This could possibly explain why obese people possibly overeat in order to compensate for their lack of reward.
 
 


== References ==
== References ==
 
{{reflist | 2}}[[Category:Suggestion Bot Tag]]
 
 
Abizaid, A. et al. (2006) Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite. J. Clin. Invest. 116, 3229–3239
 
Berridge K.C (2007). The debate over dopamine’s role in reward: the case for incentive salience. Psychopharmacology 191:391–431
 
Changizi, M. A., McGehee, R. M. & Hall, W. G. (2002). Evidence that appetitive responses for dehydration and food-deprivation are learned. Physiol. Behav. 75, 295–304.
 
Darvas, M. & Palmiter, RD.(2009) Restriction of dopamine signaling to the dorsolateral striatum is sufficient for many cognitive behaviours PNAS 106;34, 14664–14669
 
Delgado, MR. (2007) Reward-Related Responses in the Human Striatum Ann. N.Y. Acad. Sci. 1104: 70–88
 
de Wit, H. & Wise, R. A. 1977 Blockade of cocaine reinforcement in rats with the dopamine receptor blocker pimozide, but not with the noradrenergic blockers phentolamine or phenoxybenzamine. Can. J. Psychol. 31, 195–203.
 
Epstein LH, Leddy JJ, Temple JL, Faith MS (2007). Food reinforcement and eating: a multilevel analysis. Psychol Bull;133:884–906
 
Figlewicz DP. Adiposity signals and food reward: expanding the CNS roles of insulin and leptin.  American Journal of Physiology - Regulatory Integrative & Comparative Physiology. 284(4):R882-92, 2003 Apr.
 
Figlewicz DP, Benoit SC. (2009) Insulin, leptin, and food reward: update 2008.Am J Physiol Regul Integr Comp Physiol.296(1):R9-R19
 
Figlewicz DP, Bennett JL, Naleid AM, Davis C, Grimm JW. Intraventricular insulin and leptin decrease sucrose self-administration in rats.Physiol Behav 89: 611–616, 2006.
 
Figlewicz, D.P. et al. (2004).  Intraventricular insulin and leptin reverse place preference conditioned with high fat food.  Behav. Neurosci. 118, 479–48
 
Fouriezos, G. & Wise, R. A. (1976). Pimozide-induced extinction of intracranial self-stimulation: response patterns
rule out motor or performance deficits. Brain Res. 103, 377–380.
 
Johanson, I. B. & Hall, W. G. (1979). Appetitive learning in 1-day-old rat pups. Science 205, 419–421.
 
Liebman, J. M. & Butcher, L. L. (1974). Comparative involvement of dopamine and noradrenaline in rate-free
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Food intake involves both 'homeostatic feeding' (energy demands) and ‘non-homeostatic feeding’; the latter is associated with food reward, which involves both 'liking’ (pleasure/palatability) and ‘wanting’ (incentive motivation) according to the salience theory. Experiments in mice suggest that ‘liking’ involves the release of mu-opioid peptides in brain, while ‘wanting’ involves the neurotransmitter dopamine [1].


Food intake diagram.jpg
Key Definitions
Wanting/ Incentive salience - The motivational aspect of a stimulus that transforms the sensory information into a more desirable stimulus.
Liking - Immediate pleasure from consumption
Hedonia - The feeling of pleasure
Motivation- The direction towards a particular behaviour to achieve a goal
Reinforcement - The process by which a stimulus strengthens a behavioural response so that the probability of response is increased when the stimulus is presented again.

Motivated behaviour and food as a reinforcer

The brain’s reward systems react to stimuli such as sight, smell and taste, and other cues that predict food. However, hunger cannot result in unconditioned goal-directed behaviour; [2] chance encounters with palatable foods are required before goal-directed behaviour can occur, which link the internal needs with the salience of environmental stimuli [3]For exa mple, an infant recognises and learns to seek out sweet tastes, but the desire for any particular food is controlled by the interaction of peptide levels (related to hunger) with neural circuits in the brain which store the animal’s past experience of that particular food. [4] Subsequently, the infant will taste both food and non-food objects indiscriminately until it has received reinforcing feedback from enough stimuli. A monkey’s appetite for yellow bananas requires that the monkey learns to relate the sight of the yellow skin of a banana with the sweet taste of the banana, plus the consequences of eating it. Preference for a particular food results only when the post-ingestional consequences of that food ’reinforce’ the tendency to eat that food. For these reasons, food is considered to be a strong reinforcer. When the response of a behaviour stimulated by a reinforcer increases the frequency of that behaviour; that is positive reinforcement or reward learning, and the positive events are called rewards [5]. 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.


Food reward pathways

Mesolimbic Dopaminergic Reward System

The first evidence for the involvement of dopamine in food reward came from studies in rats, in which dopamine antagonists blocked the rewarding effects of brain stimulation and of psychomotor stimulants[6] [7].


The Mesolimbic Dopaminergic Reward System

In the ‘reward circuit’, projections from the ventral tegmental area (VTA) to the nucleus accumbens have received the most attention. Dopamine action in the nucleus accumbens is thought to be needed for motivation to acquire food or addictive drugs. Most reviews suggest that the projections from the VTA to the nucleus accumbens are needed for the motivation to eat, but not for food consumption itself.

The Dopamine Hypothesis
Dopamine signalling from the VTA to the nucleus accumbens, hippocampus, amygdala and/or pre-frontal cortex promotes reward-related activities. Dopamine signalling in these brain regions focuses attention to salient environmental events and facilitates behaviour towards directed goals. It is thought that dopamine released from the VTA also promotes learning between food reward and the environment.

Dopamine's role in reward?
•Hedonia – Dopamine in the nucleus accumbens has been said to act as a "pleasure" neurotransmitter. Not all rewards activate the reward system, suggesting that the mesolimbic pathway is not solely hedonic.

•Learning – predictions of future rewards, nucleus accumbens 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 dopamine, the environmental stimulus goes unnoticed and the animal will eventually die from starvation and dehydration.

The incentive salience theory seems to best fit the data in this field. Therefore dopamine causes the wanting of the reward after the appropriate stimuli have been processed in the reward system. Dopamine transmission is needed to form these associations. An increase in extracellular dopamine is seen in regard to natural rewards, food, water and sex, during acute administration. However novelty is an important factor in the increased release from the nucleus accumbens. It has been suggested that the role of dopamine in motivation is shared between the nucleus accumbens and CPu pathways(see diagram). The SNpc-CPu pathway is essential for motivation, while dopamine signalling from the VTA to the nucleus accumbens needed in regard to modulating the actions of the other dopamine pathway.

The substantia nigra pars compacta to the caudate putamen

Dopamine-deficient mice starve, apparently because they are not motivated to respond to hunger signals. Thus, it has been proposed that dopamine is crucial for mice to engage in most goal-directed or motivated behaviours. However it is not clear which dopamine pathway is involved; a universal finding is the involvement of the striatum, the input structure of the basal ganglia in a circuit responsible for mediating goal-directed behaviour, with the striatum’s central role being the processing of reward like stimuli. The two proposed pathways are from the VTA to nucleus accumbens (ventral striatum); or the substantia nigra pars compacta to the caudate putamen (dorsal striatum). The striatum includes not only the dorsal region, which encompasses the caudate nucleus and putamen, but also the ventral region that includes the core and shell of the nucleus accumbens[8]

Our understanding of how reward information is processed comes mainly from studies in animal models. One study, using nonhuman primates, found that striatal neurons responded to the anticipation and delivery of reward [9] Another found a reward-related dopamine response specifically in the mouse dorsal striatum, correlated with the delivery of food reward [10] The importance of dopamine in the dorsal striatum was demonstrated using dopamine-deficient mice whose dopamine signalling is restored by viral rescue. These mice learned to lever press for food rewards as quickly as control mice, and their motivation to work for food was restored. Importantly, in these dopamine-deficient mice, feeding was never restored after viral transduction in the nucleus accumbens.[11][12]

Recent advances in neuroimaging has allowed researchers to extend such investigations to the human brain. Dopamine is released in the dorsal striatum of hungry participants when stimulated with food items. During the delivery of rewards, fMRI signals were higher in the dorsal striatum, particularly the head of the caudate putamen(Delgado MR (2007)). It has been proposed that dopamine signaling in the caudate putamen is essential for motivation, while dopamine signaling in the nucleus accumbens modulates this motivation and evaluation of reward-like stimuli.

The effect of hormones on the dopamine reward system

Plasma concentrations of ghrelin, leptin and insulin reflect the size of energy stores, such as adipose tissue, and act at the mediobasal hypothalamus to influence appetite and energy expenditure. These hormones also affect the dopamine reward pathways [13] Receptors for these hormones are located on dopamine neurones in the VTA, and ligand binding results in activation e.g. by ghrelin [14] or inhibition e.g. by insulin or leptin of dopamine signalling to the nucleus accumbens [15]. These alterations in dopamine signalling pathways have complex effects on eating behaviours.

Both insulin and leptin attenuate food reward, reducing the incentive to eat. For example, administering insulin or leptin to rats affected conditional place preference (CPP), which assesses the ability to relate a particular food reward to a particular environment. Rats were fed a high-fat diet and underwent a ‘training period’ before the test involving intracerebroventricular administration of insulin or leptin. CPP was abolished in those rats that received insulin or leptin before or during the test as well as in training, whilst those who only received it in training maintained a normal CPP. This suggests that insulin and leptin influence the retrieval of food reward associations rather than the initial formation of these associations. These results have been reinforced by studies which have shown decreased sucrose self-administration in response to insulin or leptin, and decreased sucrose licking following insulin.[16] The high circulating concentrations of insulin and leptin associated with obesity impair dopamine food reward pathways resulting in abnormal eating behaviours.

Summary of effects of centrally administered insulin and leptin on reward behaviours

Behaviour Effect of insulin Effect of leptin
Brain self-stimulation Decrease Decrease
Relapse to heroin suckling Not tested Decrease
Acute sucrose suckling Decrease Not tested
Food-condtioned place preference Decrease Decrease
Sucrose self-administration Decrease Decrease
Acute chow intake Decrease Decrease
Opioid-stimulated sucrose Decrease Decrease
  • Adapted from Figlewicz et al. (2004)

Ghrelin can increase dopamine signalling on VTA neurones, via direct activation and also indirect manipulation of inputs onto the VTA to those of an excitatory nature. However, it is not clear whether this is a major part of the mechanism by which ghrelin stimulates feeding.[17]

Opioid and cannabinoid systems

Other reward systems, including the endogenous opioid and endocannabinoid systems interact with dopamine reward pathways. Opioid peptides act in the nucleus accumbens to increase ‘wanting’ and ‘liking’ of food rewards. [18]Opioids also influence mesolimibic dopamine pathways by inhibiting GABAergic input onto the dopamine neurones of the VTA, resulting in increased dopamine release [19]. The endocannabinoid system has also been implicated in reward behaviours, and cannabinoid receptors are expressed in several brain areas implicated in reward, including in the mesolimibic system. Endocannabinoids modulate neurotransmission, and, for example, cannabinoid agonists stimulate dopamine release. Conversly, antagonising these receptors inhibits activation of dopamine release. [20]

Food reward and obesity

There is a difference in dopamine activity between obese women and lean women/men in response to food and satiety. The obese have a higher metabolic activity in the parietal somatosensory area of the cortex which is linked to the sensory mouth, lips and tongue. Deficiencies of the dopamine D2 receptor may increase the likelihood of being obese. [21] Obese people have fewer D2 receptors in the striatum and with both the D1 and D2 receptors acting synergistically to decrease feeding, this altered expression causes increased eating. The DRD2 gene is responsible for the reinforcing properties of food/addictive behaviour. [22] Those who have the allelic variant A1 in this gene have fewer D2 receptors, making the dopamine reward circuits less sensitive.

References

  1. ↑ Berridge KC (2007) The debate over dopamine’s role in reward: the case for incentive salience. Psychopharmacology 191:391–431
  2. ↑ Changizi MA et al. (2002) Evidence that appetitive responses for dehydration and food-deprivation are learned Physiol Behav 75:295–304
  3. ↑ Wise RA (2006) Role of brain dopamine in food reward and reinforcement Phil Trans R Soc Lond B Biol Sci 361:1149–58
  4. ↑ Steiner JE et al.(2001) Comparative expression of hedonic impact: affective reactions to taste by human infants and other primates Neurosci Biobehav Rev 25:53–74
  5. ↑ Epstein LH et al.(2007) Food reinforcement and eating: a multilevel analysis Psychol Bull 133:884–906
  6. ↑ Liebman JM, Butcher LL (1974) Comparative involvement of dopamine and noradrenaline in rate-free self-stimulation in substantia nigra, lateral hypothalamus, and mesencephalic central gray N-S Arch Pharmacol
  7. ↑ Fouriezos G, Wise RA (1976) Pimozide-induced extinction of intracranial self-stimulation: response patterns rule out motor or performance deficits Brain Res 103:377–80
  8. ↑ Wickens JR et al. (2007) Striatal contributions to reward and decision making Ann NY Acad Sci 1104:192–212
  9. ↑ Delgado MR (2007) Reward-related responses in the human striatum Ann NY Acad Sci 1104: 70–88
  10. ↑ Natori S et al. (2009) Subsecond reward-related dopamine release in the mouse dorsal striatum Neurosci Res 63:267–72
  11. ↑ Darvas M, Palmiter RD (2009) Restriction of dopamine signaling to the dorsolateral striatum is sufficient for many cognitive behaviours PNAS 106;34:14664–9
  12. ↑ Palmiter RD(2008) Dopamine signaling in the dorsal striatum is essential for motivated behaviors: lessons from dopamine-deficient mice Ann N Y Acad Sci 1129:35–46
  13. ↑ Figlewicz DP, Benoit SC (2009) Insulin, leptin, and food reward: update 2008 Am J Physiol 296:R9-19
  14. ↑ Abizaid A et al. (2006) Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurones while promoting appetite J Clin Invest 116:3229–39
  15. ↑ Magni P et al. (2009) Feeding behavior in mammals including humans. Ann NY Acad Sci 1163:221-32
  16. ↑ Sipols AJ et al. (2000) Insulin and raclopride combine to decrease short-term intake of sucrose solutions. Peptides 21:1361–7
  17. ↑ Palmiter RD (2007) Is dopamine a physiologically relevant mediator of feeding behaviour? TINS 8:375-81
  18. ↑ Pecina S (2008) Opioid reward 'liking' and 'wanting' in the nucleus accumbens Physiol Behav 94:675-80
  19. ↑ Spanagel R, Weiss F (1999) The dopamine hypothesis of reward: past and current status TINS 22:521-7
  20. ↑ Solinas M (2008) The endocannabinoid system in brain reward processes Br J Pharmacol 154:369-83
  21. ↑ Wang et al. (2001) Brain dopamine and obesity. Lancet 357354-57
  22. ↑ Noble EP et al.(1994) D2 dopamine receptor gene and obesity. Int J Eating Disorders 15:205–17
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