Food reward/Bibliography: Difference between revisions

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==Review Articles==
==Review Articles==


#Magni P. ''et al.'' (2009) Feeding behavior in mammals including humans. ''Ann.N.Y.Acad.Sci.'' 1163:221-232. PMID 19456343
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
"The complex control of food intake and energy metabolism in mammals relies on the
ability of the brain to integrate multiple signals indicating the nutritional state and
the energy level of the organism and to produce appropriate responses in terms of
food intake, energy expenditure, andmetabolic activity. Central regulation of feeding is
organized as a long-loop mechanism involving humoral signals and afferent neuronal
pathways to the brain"
Palmiter R. (2007) Is dopamine a physiologically relevant mediator of feeding behaviour TINS 30;8
The hypothalamus integrates various hormonal and neuronal signals to regulate appetite and metabolism and thereby serves a homeostatic purpose in the regulation of body weight. Additional neural circuits that are superimposed on this system have the potential to override the homeostatic signals, resulting in either gluttony or anorexia at the extremes. Midbrain dopamine neurons have long been implicated in mediating reward behavior and the motivational aspects of feeding behavior. Recent results reveal that hormones implicated in regulating the homeostatic system also impinge directly on dopamine neurons; for example, leptin and insulin directly inhibit dopamine neurons, whereas ghrelin activates them. Here, I discuss the predictions and implications of these new findings as they relate to dopamine signaling and the physiology of appetite control.


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.


Spanagel, R. Weiss, F. (1999) The dopamine hypothesis of reward:past and current status TINS 22(11)
Darvas, M. & Palmiter, RD.(2009) Restriction of dopamine signaling to the dorsolateral striatum is sufficient for many cognitive behaviours PNAS 106;34, 14664–14669
Mesolimbic dopaminergic neurons are thought to serve as a final common neural pathway for
mediating reinforcement processes.However,several recent findings have challenged the view that mesolimbic dopamine has a crucial role in the maintenance of reinforcement processes, or the subjective rewarding actions of natural rewards and drugs of abuse. Instead, there is growing evidence that dopamine is involved in the formation of associations between salient contextual stimuli and internal rewarding or aversive events.This evidence suggests that dopaminergic-neuron activation aids the organism in learning to recognize stimuli associated with such events.Thus, mesolimbic dopaminergic neurons have an important function in the acquisition of behavior reinforced by natural reward and drug stimuli. Furthermore, long-lasting neuroadaptive changes in mesolimbic dopamine-mediated transmission that develop during chronic drug use might contribute to compulsive drug-seeking behavior and relapse.


Epstein L.H. et al (2007) Food reinforcement and Eating: A Multilevel analysis. Pyschol Bull 133(5)884-906
Delgado, MR. (2007) Reward-Related Responses in the Human Striatum Ann. N.Y. Acad. Sci. 1104: 70–88
Eating represents a choice among many alternative behaviors. The purpose of this review is to provide an overview of how food reinforcement and behavioral choice theory are related to eating and to show how this theoretical approach may help organize research on eating from molecular genetics through treatment and prevention of obesity. Special emphasis is placed on how food reinforcement and behavioral choice theory are relevant to understanding excess energy intake and obesity and how they provide a framework for examining factors that may influence eating and are outside of those that may regulate energy homeostasis. Methods to measure food reinforcement are reviewed, along with factors that influence the reinforcing value of eating. Contributions of neuroscience and genetics to the study of food reinforcement are illustrated by using the example of dopamine. Implications of
food reinforcement for obesity and positive energy balance are explored, with suggestions for novel approaches to obesity treatment based on the synthesis of behavioral and pharmacological approaches to food reinforcement.


Wise, R.A. (2006) Role of brain dopamine in food reward and reinforcement. Phil. Trans. R. Soc. B (2006) 361, 1149–1158
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.
The ability of food to establish and maintain response habits and conditioned preferences depends largely on the function of brain dopamine systems. While dopaminergic transmission in the nucleus accumbens appears sufficient for some forms of reward, the role of dopamine in food reward does not appear to be restricted to this region. Dopamine plays an important role in both the ability to energize feeding and to reinforce food-seeking behaviour; the role in energizing feeding is secondary to the prerequisite role in reinforcement. Dopaminergic activation is triggered by the auditory and visual as
 
well as the tactile, olfactory, and gustatory stimuli of foods. While dopamine plays a central role in the feeding and food-seeking of normal animals, some food rewarded learning can be seen in genetically engineered dopamine-deficient mice.
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, Benoit SC. (2009) Insulin, leptin, and food reward: update 2008.Am J Physiol Regul Integr Comp Physiol.296(1):R9-R19
The hormones insulin and leptin have been demonstrated to act in the central nervous system (CNS) as regulators of energy homeostasis at medial hypothalamic sites. In a previous review, we described new research demonstrating that, in addition to these direct homeostatic actions at the hypothalamus, CNS circuitry that subserves reward and motivation is also a direct and an indirect target for insulin and leptin action. Specifically, insulin and leptin can decrease food reward behaviors and modulate the function of neurotransmitter systems and neural circuitry that mediate food reward, i.e., midbrain dopamine and opioidergic pathways. Here we summarize new behavioral, systems, and cellular evidence in support of this hypothesis and in the context of research into the homeostatic roles of both hormones in the CNS. We discuss some current issues in the field that should provide additional insight into this hypothetical model. The understanding of neuroendocrine modulation of food reward, as well as food reward modulation by diet and obesity, may point to new directions for therapeutic approaches to overeating or eating disorders.
 
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
 
 
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
self-stimulation in substantia nigra, lateral hypothalamus, and mesencephalic central gray. N-S. Arch. Pharmacol.
 
Magni P. et al. (2009) Feeding behavior in mammals including humans. Ann.N.Y.Acad.Sci. 1163:221-232
 
Maldonado, R et al (2006). Involvement of the endocannabinoid system in drug addiction. Trends Neurosci; 29, 225-232.
 
Natori, S. Yoshimi K. Takahashi T. Kagohashi M. Oyama G. Shimo  Y. Hattori N. Kitazawa S. (2009) Subsecond reward-related dopamine release in the mouse dorsal striatum . Neuroscience Research 63, 267–272
 
Noble EP, Noble RE, Ritchie T, Syndulko K, Bohlman MC, Noble LA, et al. D2 dopamine receptor gene and obesity. International Journal of Eating Disorders 1994;15:205–217.
 
Palmiter R.D (2007) Is dopamine a physiologically relevant mediator of feeding behaviour? TINS 30. 8:375-381
 
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.
 
Pecina s. Opioid reward 'liking' and 'wanting' in the nucleus accumbens.  Physiology & Behavior. 94(5):675-80, 2008 Aug 6.
 
Spanagel R & Weiss F (1999). The dopamine hypothesis of reward: past and current status. TINS. 22.11: 521-527
 
Satoh, T. Nakai, S. Sato T., Kimura M. (2003) Correlated Coding of Motivation and Outcome of Decision by dopamine neurons. The Journal of Neuroscience, 23(30):9913–9923
 
Sipols AJ, Stuber GD, Klein SN, Higgins MS, Figlewicz DP. Insulin and raclopride combine to decrease short-term intake of sucrose solutions.  Peptides 21: 1361–1367, 2000.
 
Spanagel R and Weiss F.  The dopamine hypothesis of reward: past and current status.  Trends Neurosci. (1999) 22, 521-527.
 
Steiner, J. E., Glaser, D., Hawilo, M. E. & Berridge, K. C. (2001). Comparative expression of hedonic impact: affective
reactions to taste by human infants and other primates.Neurosci. Biobehav. Rev. 25, 53–74.
 
Wang et al (2001) Brain dopamine and obesity. The Lancet • Vol 357, 354-357
 
Wickens, JR. Budd, CS. Hyland, BI. Arbuthnott, GW. (2007) Striatal Contributions to Reward and Decision Making Ann. N.Y. Acad. Sci. 1104: 192–212 <br />
 
Wise RA (2006). Role of brain dopamine in food reward and reinforcement. Philos Trans R Soc Lond B Biol Sci;361:1149–1158.
 
Wise, R. A. (2004b). Drive, incentive, and reinforcement: the antecedents and consequences of motivation. Nebr. Symp.
Motiv. 50, 159–195.
 
Wise RA & Rompre PP (1989). Annual review Psychology. 40: 191-225


==Primary Research Papers==
==Primary Research Papers==

Revision as of 08:19, 15 November 2009

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A list of key readings about Food reward.
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Review Articles

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


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 self-stimulation in substantia nigra, lateral hypothalamus, and mesencephalic central gray. N-S. Arch. Pharmacol.

Magni P. et al. (2009) Feeding behavior in mammals including humans. Ann.N.Y.Acad.Sci. 1163:221-232

Maldonado, R et al (2006). Involvement of the endocannabinoid system in drug addiction. Trends Neurosci; 29, 225-232.

Natori, S. Yoshimi K. Takahashi T. Kagohashi M. Oyama G. Shimo Y. Hattori N. Kitazawa S. (2009) Subsecond reward-related dopamine release in the mouse dorsal striatum . Neuroscience Research 63, 267–272

Noble EP, Noble RE, Ritchie T, Syndulko K, Bohlman MC, Noble LA, et al. D2 dopamine receptor gene and obesity. International Journal of Eating Disorders 1994;15:205–217.

Palmiter R.D (2007) Is dopamine a physiologically relevant mediator of feeding behaviour? TINS 30. 8:375-381

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.

Pecina s. Opioid reward 'liking' and 'wanting' in the nucleus accumbens. Physiology & Behavior. 94(5):675-80, 2008 Aug 6.

Spanagel R & Weiss F (1999). The dopamine hypothesis of reward: past and current status. TINS. 22.11: 521-527

Satoh, T. Nakai, S. Sato T., Kimura M. (2003) Correlated Coding of Motivation and Outcome of Decision by dopamine neurons. The Journal of Neuroscience, 23(30):9913–9923

Sipols AJ, Stuber GD, Klein SN, Higgins MS, Figlewicz DP. Insulin and raclopride combine to decrease short-term intake of sucrose solutions. Peptides 21: 1361–1367, 2000.

Spanagel R and Weiss F. The dopamine hypothesis of reward: past and current status. Trends Neurosci. (1999) 22, 521-527.

Steiner, J. E., Glaser, D., Hawilo, M. E. & Berridge, K. C. (2001). Comparative expression of hedonic impact: affective reactions to taste by human infants and other primates.Neurosci. Biobehav. Rev. 25, 53–74.

Wang et al (2001) Brain dopamine and obesity. The Lancet • Vol 357, 354-357

Wickens, JR. Budd, CS. Hyland, BI. Arbuthnott, GW. (2007) Striatal Contributions to Reward and Decision Making Ann. N.Y. Acad. Sci. 1104: 192–212

Wise RA (2006). Role of brain dopamine in food reward and reinforcement. Philos Trans R Soc Lond B Biol Sci;361:1149–1158.

Wise, R. A. (2004b). Drive, incentive, and reinforcement: the antecedents and consequences of motivation. Nebr. Symp. Motiv. 50, 159–195.

Wise RA & Rompre PP (1989). Annual review Psychology. 40: 191-225

Primary Research Papers

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