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
Berridge KC (2007). The debate over dopamine’s role in reward: the case for incentive salience ''Psychopharmacology'' 191:391–431
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, processing in hypothalamic neuronal circuits, and descending
commands using vagal and spinal neurons. Sensor mechanisms or receptors sensitive
to glucose and fatty acid metabolism, neuropeptide and cannabinoid receptors, as well
as neurotransmitters and neuromodulators synthesized and secreted within the brain
itself are all signals integrated in the hypothalamus, which therefore functions as an integrator of signals from central and peripheral structures. Homeostatic feedback mechanisms involving afferent neuroendocrine inputs from peripheral organs, like adipose
tissue, gut, stomach, endocrine pancreas, adrenal, muscle, and liver, to hypothalamic
sites thus contribute to themaintenance of normal feeding behavior and energy balance.
In addition to transcriptional events, peripheral hormones may also alter firing and/or
connection (synaptology) of hypothalamic neuronal networks in order tomodulate food
intake. Moreover, intracellular energy sensing and subsequent biochemical adaptations,
including an increase in AMP-activated protein kinase activity, occur in hypothalamic
neurons. Understanding the regulation of appetite is clearly a major research effort but
also seems promising for the development of novel therapeutic strategies for obesity.


Palmiter R. (2007) Is dopamine a physiologically relevant mediator of feeding behaviour TINS 30;8
Changizi MA ''et al.''(2002). Evidence that appetitive responses for dehydration and food-deprivation are learned. Physiol. Behav. 75, 295–304.
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.


Delgado, MR. (2007) Reward-related responses in the human striatum ''Ann NY Acad Sci'' 1104:70–88


de Wit H, Wise RA (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.


Spanagel, R. Weiss, F. (1999) The dopamine hypothesis of reward:past and current status TINS 22(11)
Epstein LH ''et al.''(2007) Food reinforcement and eating: a multilevel analysis ''Psychol Bull'' 133:884–906
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
Figlewicz DP (2003) Adiposity signals and food reward: expanding the CNS roles of insulin and leptin  ''Am J Physiol'' 284:R882-92
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
Figlewicz DP, Benoit SC (2009) Insulin, leptin, and food reward: update ''Am J Physiol'' 296:R9-R19
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.


Figlewicz DP, Benoit SC. (2009) Insulin, leptin, and food reward: update 2008.Am J Physiol Regul Integr Comp Physiol.296(1):R9-R19
Johanson IB, Hall WG (1979) Appetitive learning in 1-day-old rat pups ''Science'' 205:419–421.
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.
 
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''
 
Magni P ''et al.'' (2009) Feeding behavior in mammals including humans ''Ann N Y Acad.Sci'' 1163:221-32
 
Maldonado, R et al (2006). Involvement of the endocannabinoid system in drug addiction.  ''Trends Neurosci'' 29:225-32.
 
Natori S ''et al.'' (2009) Subsecond reward-related dopamine release in the mouse dorsal striatum ''Neurosci Res'' 63:267–72
 
Noble EP ''et al.'' (1994) D2 dopamine receptor gene and obesity. ''Int J Eating Disorders'' 15:205–217
 
Palmiter RD (2007) Is dopamine a physiologically relevant mediator of feeding behaviour? ''TINS'' 30. 8:375-81
 
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  (2008) Opioid reward 'liking' and 'wanting' in the nucleus accumbens  ''Physiol Behav'' 94(5):675-80
 
Solinas M (2008) 'The endocannabinoid system in brain reward processes. ''Br J Pharmacol'' 154:369-83.
 
Spanagel R & Weiss F (1999). The dopamine hypothesis of reward: past and current status. TINS. 22.11: 521-7
 
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
 
Spanagel R and Weiss F (1999) The dopamine hypothesis of reward: past and current status.  ''Trends Neurosci'' 22:521-7.
 
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
 
Wang ''et al.'' (2001) Brain dopamine and obesity ''The Lancet'' 357:354-7
 
Wickens JR ''et al.'' (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'' 361:1149–58.
 
Wise RA (2004b) Drive, incentive, and reinforcement: the antecedents and consequences of motivation. ''Nebr Symp
Motiv'' 50, 159–195.
 
Wise RA & Rompre PP (1989). ''Ann rev Psychol'' 40: 191-225


==Primary Research Papers==
==Primary Research Papers==
Abizaid A ''et al.'' (2006) Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite ''J Clin Invest'' 116:3229–39
Darvas M, Palmiter RD (2009) Restriction of dopamine signaling to the dorsolateral striatum is sufficient for many cognitive behaviours ''PNAS'' 106;34, 14664–14669
Figlewicz DP ''et al.'' Intraventricular insulin and leptin decrease sucrose self-administration in rats ''Physiol Behav'' 89:611–616, 2006.
Figlewicz DP ''et al.'' (2004) Intraventricular insulin and leptin reverse place preference conditioned with high fat food. ''Behav Neurosci'' 118:479–48
Fouriezos G, Wise RA (1976) Pimozide-induced extinction of intracranial self-stimulation: response patterns rule out motor or performance deficits. ''Brain Res'' 103, 377–380.
Sipols AJ ''et al.'' (2000) Insulin and raclopride combine to decrease short-term intake of sucrose solutions  ''Peptides'' 21:1361–7

Latest revision as of 12:33, 19 August 2012

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Review Articles

Berridge KC (2007). The debate over dopamine’s role in reward: the case for incentive salience Psychopharmacology 191:391–431

Changizi MA et al.(2002). Evidence that appetitive responses for dehydration and food-deprivation are learned. Physiol. Behav. 75, 295–304.

Delgado, MR. (2007) Reward-related responses in the human striatum Ann NY Acad Sci 1104:70–88

de Wit H, Wise RA (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 et al.(2007) Food reinforcement and eating: a multilevel analysis Psychol Bull 133:884–906

Figlewicz DP (2003) Adiposity signals and food reward: expanding the CNS roles of insulin and leptin Am J Physiol 284:R882-92

Figlewicz DP, Benoit SC (2009) Insulin, leptin, and food reward: update Am J Physiol 296:R9-R19

Johanson IB, Hall WG (1979) Appetitive learning in 1-day-old rat pups Science 205:419–421.

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

Magni P et al. (2009) Feeding behavior in mammals including humans Ann N Y Acad.Sci 1163:221-32

Maldonado, R et al (2006). Involvement of the endocannabinoid system in drug addiction. Trends Neurosci 29:225-32.

Natori S et al. (2009) Subsecond reward-related dopamine release in the mouse dorsal striatum Neurosci Res 63:267–72

Noble EP et al. (1994) D2 dopamine receptor gene and obesity. Int J Eating Disorders 15:205–217

Palmiter RD (2007) Is dopamine a physiologically relevant mediator of feeding behaviour? TINS 30. 8:375-81

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 (2008) Opioid reward 'liking' and 'wanting' in the nucleus accumbens Physiol Behav 94(5):675-80

Solinas M (2008) 'The endocannabinoid system in brain reward processes. Br J Pharmacol 154:369-83.

Spanagel R & Weiss F (1999). The dopamine hypothesis of reward: past and current status. TINS. 22.11: 521-7

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

Spanagel R and Weiss F (1999) The dopamine hypothesis of reward: past and current status. Trends Neurosci 22:521-7.

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

Wang et al. (2001) Brain dopamine and obesity The Lancet 357:354-7

Wickens JR et al. (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 361:1149–58.

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

Wise RA & Rompre PP (1989). Ann rev Psychol 40: 191-225

Primary Research Papers

Abizaid A et al. (2006) Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite J Clin Invest 116:3229–39

Darvas M, Palmiter RD (2009) Restriction of dopamine signaling to the dorsolateral striatum is sufficient for many cognitive behaviours PNAS 106;34, 14664–14669

Figlewicz DP et al. Intraventricular insulin and leptin decrease sucrose self-administration in rats Physiol Behav 89:611–616, 2006.

Figlewicz DP et al. (2004) Intraventricular insulin and leptin reverse place preference conditioned with high fat food. Behav Neurosci 118:479–48

Fouriezos G, Wise RA (1976) Pimozide-induced extinction of intracranial self-stimulation: response patterns rule out motor or performance deficits. Brain Res 103, 377–380.

Sipols AJ et al. (2000) Insulin and raclopride combine to decrease short-term intake of sucrose solutions Peptides 21:1361–7

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