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Article ; Online: Dopamine, behavior, and addiction.

Wise, Roy A / Jordan, Chloe J

2021 Volume 28, Issue 1, Page(s) 83

Abstract: Addictive drugs are habit-forming. Addiction is a learned behavior; repeated exposure to addictive drugs can stamp in learning. Dopamine-depleted or dopamine-deleted animals have only unlearned reflexes; they lack learned seeking and learned avoidance. ... ...

Abstract	Addictive drugs are habit-forming. Addiction is a learned behavior; repeated exposure to addictive drugs can stamp in learning. Dopamine-depleted or dopamine-deleted animals have only unlearned reflexes; they lack learned seeking and learned avoidance. Burst-firing of dopamine neurons enables learning-long-term potentiation (LTP)-of search and avoidance responses. It sets the stage for learning that occurs between glutamatergic sensory inputs and GABAergic motor-related outputs of the striatum; this learning establishes the ability to search and avoid. Independent of burst-firing, the rate of single-spiking-or "pacemaker firing"-of dopaminergic neurons mediates motivational arousal. Motivational arousal increases during need states and its level determines the responsiveness of the animal to established predictive stimuli. Addictive drugs, while usually not serving as an external stimulus, have varying abilities to activate the dopamine system; the comparative abilities of different addictive drugs to facilitate LTP is something that might be studied in the future.
MeSH term(s)	Animals ; Appetitive Behavior/drug effects ; Avoidance Learning/drug effects ; Behavior, Addictive/psychology ; Dopamine/deficiency ; Dopaminergic Neurons/metabolism ; Learning/drug effects ; Long-Term Potentiation ; Mice ; Rats ; Reflex/drug effects
Chemical Substances	Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2021-12-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-021-00779-7
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Zs.A 4037: Show issues

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Article ; Online: Dopamine and Addiction.

Wise, Roy A / Robble, Mykel A

Annual review of psychology

2020 Volume 71, Page(s) 79–106

Abstract: Addiction is commonly identified with habitual nonmedical self-administration of drugs. It is usually defined by characteristics of intoxication or by characteristics of withdrawal symptoms. Such addictions can also be defined in terms of the brain ... ...

Abstract	Addiction is commonly identified with habitual nonmedical self-administration of drugs. It is usually defined by characteristics of intoxication or by characteristics of withdrawal symptoms. Such addictions can also be defined in terms of the brain mechanisms they activate; most addictive drugs cause elevations in extracellular levels of the neurotransmitter dopamine. Animals unable to synthesize or use dopamine lack the conditioned reflexes discussed by Pavlov or the appetitive behavior discussed by Craig; they have only unconditioned consummatory reflexes. Burst discharges (phasic firing) of dopamine-containing neurons are necessary to establish long-term memories associating predictive stimuli with rewards and punishers. Independent discharges of dopamine neurons (tonic or pacemaker firing) determine the motivation to respond to such cues. As a result of habitual intake of addictive drugs, dopamine receptors expressed in the brain are decreased, thereby reducing interest in activities not already stamped in by habitual rewards.
MeSH term(s)	Animals ; Behavior, Addictive/metabolism ; Dopamine/metabolism ; Dopaminergic Neurons/physiology ; Humans ; Memory, Long-Term/physiology ; Motivation/physiology ; Receptors, Dopamine/metabolism ; Reward
Chemical Substances	Receptors, Dopamine ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2020-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	207937-9
ISSN	1545-2085 ; 0066-4308 ; 0547-1567
ISSN (online)	1545-2085
ISSN	0066-4308 ; 0547-1567
DOI	10.1146/annurev-psych-010418-103337
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Zs.A 1743: Show issues

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Article ; Online: Dual roles of dopamine in food and drug seeking: the drive-reward paradox.

Wise, Roy A

Biological psychiatry

2012 Volume 73, Issue 9, Page(s) 819–826

Abstract: The question of whether (or to what degree) obesity reflects addiction to high-energy foods often narrows to the question of whether the overeating of these foods causes the same long-term neuroadaptations as are identified with the late stages of ... ...

Abstract	The question of whether (or to what degree) obesity reflects addiction to high-energy foods often narrows to the question of whether the overeating of these foods causes the same long-term neuroadaptations as are identified with the late stages of addiction. Of equal or perhaps greater interest is the question of whether common brain mechanisms mediate the acquisition and development of eating and drug-taking habits. The earliest evidence on this question is rooted in early studies of brain stimulation reward. Lateral hypothalamic electrical stimulation can be reinforcing in some conditions and can motivate feeding in others. That stimulation of the same brain region should be both reinforcing and drive inducing is paradoxical; why should an animal work to induce a drive-like state such as hunger? This is known as the drive-reward paradox. Insights into the substrates of the drive-reward paradox suggest an answer to the controversial question of whether the dopamine system--a system downstream from the stimulated fibers of the lateral hypothalamus--is more critically involved in wanting or in liking of various rewards including food and addictive drugs. That the same brain circuitry is implicated in the motivation for and the reinforcement by both food and addictive drugs extends the argument for a common mechanism underlying compulsive overeating and compulsive drug taking.
MeSH term(s)	Behavior, Addictive/physiopathology ; Brain/physiopathology ; Dopamine/physiology ; Drive ; Drug-Seeking Behavior/physiology ; Feeding Behavior/physiology ; Food ; Humans ; Reward
Chemical Substances	Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2012-10-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2012.09.001
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Zs.A 720: Show issues

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Article ; Online: Lateral hypothalamic circuits for feeding and reward.

Stuber, Garret D / Wise, Roy A

Nature neuroscience

2016 Volume 19, Issue 2, Page(s) 198–205

Abstract: In experiments conducted over 60 years ago, the lateral hypothalamic area (LHA) was identified as a critical neuroanatomical substrate for motivated behavior. Electrical stimulation of the LHA induces voracious feeding even in well-fed animals. In the ... ...

Abstract	In experiments conducted over 60 years ago, the lateral hypothalamic area (LHA) was identified as a critical neuroanatomical substrate for motivated behavior. Electrical stimulation of the LHA induces voracious feeding even in well-fed animals. In the absence of food, animals will work tirelessly, often lever-pressing thousands of times per hour, for electrical stimulation at the same site that provokes feeding, drinking and other species-typical motivated behaviors. Here we review the classic findings from electrical stimulation studies and integrate them with more recent work that has used contemporary circuit-based approaches to study the LHA. We identify specific anatomically and molecularly defined LHA elements that integrate diverse information arising from cortical, extended amygdala and basal forebrain networks to ultimately generate a highly specified and invigorated behavioral state conveyed via LHA projections to downstream reward and feeding-specific circuits.
MeSH term(s)	Animals ; Electric Stimulation ; Feeding Behavior/physiology ; Humans ; Hypothalamic Area, Lateral/physiology ; Motivation ; Neural Pathways/physiology ; Reward
Language	English
Publishing date	2016-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/nn.4220
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Zs.A 4891: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 67: Show issues

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Article ; Online: Roles for nigrostriatal--not just mesocorticolimbic--dopamine in reward and addiction.

Wise, Roy A

Trends in neurosciences

2009 Volume 32, Issue 10, Page(s) 517–524

Abstract: Forebrain dopamine circuitry has traditionally been studied by two largely independent specialist groups: students of Parkinson's disease who study the nigrostriatal dopamine system that originates in the substantia nigra (SN), and students of motivation ...

Abstract	Forebrain dopamine circuitry has traditionally been studied by two largely independent specialist groups: students of Parkinson's disease who study the nigrostriatal dopamine system that originates in the substantia nigra (SN), and students of motivation and addiction who study the role of the mesolimbic and mesocortical dopamine systems that originate in the ventral tegmental area (VTA). The anatomical evidence for independent nigrostriatal and mesolimbic dopamine systems has, however, long been obsolete. There is now compelling evidence that both nominal "systems" participate in reward function and addiction. Electrical stimulation of both SN and VTA is rewarding, blockade of glutamatergic or cholinergic input to either SN or VTA attenuates the habit-forming effects of intravenous cocaine, and dopamine in both nigrostriatal and mesocorticolimbic terminal fields participates in the defining property of rewarding events: the reinforcement of memory consolidation. Thus, the similarities between nigrostriatal and mesolimbic dopamine systems can be as important as their differences.
MeSH term(s)	Animals ; Behavior, Addictive ; Cerebral Cortex/physiology ; Cocaine/administration & dosage ; Cocaine/pharmacology ; Corpus Striatum/drug effects ; Corpus Striatum/physiology ; Dopamine/physiology ; Dopamine Agonists/administration & dosage ; Dopamine Agonists/pharmacology ; Dopamine Antagonists/administration & dosage ; Dopamine Antagonists/pharmacology ; Humans ; Infusions, Intravenous ; Long-Term Potentiation/drug effects ; Long-Term Potentiation/physiology ; Long-Term Synaptic Depression/drug effects ; Long-Term Synaptic Depression/physiology ; Microinjections ; Neural Pathways/anatomy & histology ; Neural Pathways/physiology ; Reinforcement, Psychology ; Reward ; Self Stimulation/drug effects ; Self Stimulation/physiology ; Substantia Nigra/drug effects ; Substantia Nigra/physiology ; Ventral Tegmental Area/drug effects ; Ventral Tegmental Area/physiology
Chemical Substances	Dopamine Agonists ; Dopamine Antagonists ; Cocaine (I5Y540LHVR) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2009-09-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	282488-7
ISSN	1878-108X ; 0378-5912 ; 0166-2236
ISSN (online)	1878-108X
ISSN	0378-5912 ; 0166-2236
DOI	10.1016/j.tins.2009.06.004
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Zs.A 1442: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 53: Show issues

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Article: Ventral tegmental glutamate: a role in stress-, cue-, and cocaine-induced reinstatement of cocaine-seeking.

Wise, Roy A

Neuropharmacology

2008 Volume 56 Suppl 1, Page(s) 174–176

Abstract: Ventral tegmental dopamine neurons are activated by primary rewards and, when such rewards are predictable' by reward-predicting stimuli. Glutamatergic input to the ventral tegmental area contributes to this activation: in animals trained to self- ... ...

Abstract	Ventral tegmental dopamine neurons are activated by primary rewards and, when such rewards are predictable' by reward-predicting stimuli. Glutamatergic input to the ventral tegmental area contributes to this activation: in animals trained to self-administer cocaine, cocaine-predictive cues trigger ventral tegmental glutamate release and dopaminergic activation. Mild footshock stress similarly causes glutamate release and dopaminergic activation in cocaine-trained but not cocaine-naïve animals. The ability of cocaine-predictive and stress-associated cues to activate the dopamine system and to trigger cocaine craving appears to be related to changes in the ability of glutamate to activate dopaminergic neurons, changes known to be caused by experience with stress or with drugs of abuse.
MeSH term(s)	Animals ; Cocaine/administration & dosage ; Cocaine-Related Disorders/etiology ; Cocaine-Related Disorders/pathology ; Cocaine-Related Disorders/psychology ; Cues ; Glutamic Acid/metabolism ; Humans ; Stress, Psychological/complications ; Ventral Tegmental Area/drug effects ; Ventral Tegmental Area/metabolism
Chemical Substances	Glutamic Acid (3KX376GY7L) ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	2008-06-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2008.06.008
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Article: Dopamine and reward: the anhedonia hypothesis 30 years on.

Wise, Roy A

Neurotoxicity research

2008 Volume 14, Issue 2-3, Page(s) 169–183

Abstract: The anhedonia hypothesis--that brain dopamine plays a critical role in the subjective pleasure associated with positive rewards--was intended to draw the attention of psychiatrists to the growing evidence that dopamine plays a critical role in the ... ...

Abstract	The anhedonia hypothesis--that brain dopamine plays a critical role in the subjective pleasure associated with positive rewards--was intended to draw the attention of psychiatrists to the growing evidence that dopamine plays a critical role in the objective reinforcement and incentive motivation associated with food and water, brain stimulation reward, and psychomotor stimulant and opiate reward. The hypothesis called to attention the apparent paradox that neuroleptics, drugs used to treat a condition involving anhedonia (schizophrenia), attenuated in laboratory animals the positive reinforcement that we normally associate with pleasure. The hypothesis held only brief interest for psychiatrists, who pointed out that the animal studies reflected acute actions of neuroleptics whereas the treatment of schizophrenia appears to result from neuroadaptations to chronic neuroleptic administration, and that it is the positive symptoms of schizophrenia that neuroleptics alleviate, rather than the negative symptoms that include anhedonia. Perhaps for these reasons, the hypothesis has had minimal impact in the psychiatric literature. Despite its limited heuristic value for the understanding of schizophrenia, however, the anhedonia hypothesis has had major impact on biological theories of reinforcement, motivation, and addiction. Brain dopamine plays a very important role in reinforcement of response habits, conditioned preferences, and synaptic plasticity in cellular models of learning and memory. The notion that dopamine plays a dominant role in reinforcement is fundamental to the psychomotor stimulant theory of addiction, to most neuroadaptation theories of addiction, and to current theories of conditioned reinforcement and reward prediction. Properly understood, it is also fundamental to recent theories of incentive motivation.
MeSH term(s)	Animals ; Antipsychotic Agents/pharmacology ; Antipsychotic Agents/therapeutic use ; Behavior, Addictive ; Dopamine/pharmacology ; Dopamine/physiology ; Humans ; Models, Psychological ; Motivation ; Nucleus Accumbens/drug effects ; Nucleus Accumbens/physiology ; Philosophy ; Rats ; Reinforcement, Psychology ; Reward ; Schizophrenia/physiopathology
Chemical Substances	Antipsychotic Agents ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2008-12-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2036826-4
ISSN	1476-3524 ; 1029-8428
ISSN (online)	1476-3524
ISSN	1029-8428
DOI	10.1007/BF03033808
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Zs.A 5749: Show issues

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Article ; Online: Drive and Reinforcement Circuitry in the Brain: Origins, Neurotransmitters, and Projection Fields.

Wise, Roy A / McDevitt, Ross A

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2017 Volume 43, Issue 4, Page(s) 680–689

Abstract: Brain stimulation has identified two central subsets of stimulation sites with motivational relevance. First, there is a large and disperse set of sites where stimulation is reinforcing, increasing the frequency of the responses it follows, and second, a ...

Abstract	Brain stimulation has identified two central subsets of stimulation sites with motivational relevance. First, there is a large and disperse set of sites where stimulation is reinforcing, increasing the frequency of the responses it follows, and second, a much more restricted set of sites where-along with reinforcement-stimulation also has drive-like effects, instigating feeding, copulation, predation, and other motivated acts in otherwise sated or peaceful animals. From this work a dispersed but synaptically interconnected network of reinforcement circuitry is emerging: it includes afferents to the ventral tegmental area and substantia nigra; the dopamine systems themselves; glutamatergic afferents to the striatum; and one of two dopamine-receptor-expressing efferent pathways of the striatum. Stimulation of a limited subset of these sites, including descending inhibitory medial forebrain bundle fibers, induces both feeding and reinforcement, and suggests the possibility of a subset of fibers where stimulation has both drive-like and reinforcing effects. This review stresses the common findings of sites and connectivity between electrical and optogenetic studies of core drive and reinforcement sites. By doing so, it suggests the biological importance of optogenetic follow-up of less-publicized electrical stimulation findings. Such studies promise not only information about origins, neurotransmitters, and connectivity of related networks, by covering more sensory and at least one putative motor component they also promote a much deeper understanding of the breadth of motivational function.
MeSH term(s)	Animals ; Brain/physiology ; Corpus Striatum/physiology ; Humans ; Motivation/physiology ; Nerve Net/physiology ; Neural Pathways/physiology ; Neurotransmitter Agents/physiology ; Reinforcement (Psychology) ; Reward ; Substantia Nigra/physiology ; Ventral Tegmental Area/physiology
Chemical Substances	Neurotransmitter Agents
Language	English
Publishing date	2017-10-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/npp.2017.228
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Zs.A 2379: Show issues

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Article ; Online: The dopamine motive system: implications for drug and food addiction.

Volkow, Nora D / Wise, Roy A / Baler, Ruben

Nature reviews. Neuroscience

2017 Volume 18, Issue 12, Page(s) 741–752

Abstract: Behaviours such as eating, copulating, defending oneself or taking addictive drugs begin with a motivation to initiate the behaviour. Both this motivational drive and the behaviours that follow are influenced by past and present experience with the ... ...

Abstract	Behaviours such as eating, copulating, defending oneself or taking addictive drugs begin with a motivation to initiate the behaviour. Both this motivational drive and the behaviours that follow are influenced by past and present experience with the reinforcing stimuli (such as drugs or energy-rich foods) that increase the likelihood and/or strength of the behavioural response (such as drug taking or overeating). At a cellular and circuit level, motivational drive is dependent on the concentration of extrasynaptic dopamine present in specific brain areas such as the striatum. Cues that predict a reinforcing stimulus also modulate extrasynaptic dopamine concentrations, energizing motivation. Repeated administration of the reinforcer (drugs, energy-rich foods) generates conditioned associations between the reinforcer and the predicting cues, which is accompanied by downregulated dopaminergic response to other incentives and downregulated capacity for top-down self-regulation, facilitating the emergence of impulsive and compulsive responses to food or drug cues. Thus, dopamine contributes to addiction and obesity through its differentiated roles in reinforcement, motivation and self-regulation, referred to here as the 'dopamine motive system', which, if compromised, can result in increased, habitual and inflexible responding. Thus, interventions to rebalance the dopamine motive system might have therapeutic potential for obesity and addiction.
Language	English
Publishing date	2017-11-16
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2034150-7
ISSN	1471-0048 ; 1471-0048 ; 1471-003X
ISSN (online)	1471-0048
ISSN	1471-0048 ; 1471-003X
DOI	10.1038/nrn.2017.130
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Zs.A 5473: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Cocaine and cocaine expectancy increase growth hormone, ghrelin, GLP-1, IGF-1, adiponectin, and corticosterone while decreasing leptin, insulin, GIP, and prolactin.

You, Zhi-Bing / Wang, Bin / Gardner, Eliot L / Wise, Roy A

Pharmacology, biochemistry, and behavior

2018 Volume 176, Page(s) 53–56

Abstract: The dopamine system-essential for mood and movement-can be activated in two ways: by excitatory inputs that cause burst firing and stamp-in learning or by slow excitatory or inhibitory inputs-like leptin, insulin, ghrelin, or corticosterone-that decrease ...

Abstract	The dopamine system-essential for mood and movement-can be activated in two ways: by excitatory inputs that cause burst firing and stamp-in learning or by slow excitatory or inhibitory inputs-like leptin, insulin, ghrelin, or corticosterone-that decrease or increase single-spike (pacemaker) firing rate and that modulate motivation. In the present study we monitored blood samples taken prior to and during intravenous cocaine or saline self-administration in rats. During cocaine-taking, growth hormone and acetylated ghrelin increased 10-fold; glucagon-like peptide-1 (GLP-1) doubled; non-acetylated ghrelin, insulin-like growth factor-1 (IGF-1), and corticosterone increased by 50% and adiponectin increased by 17%. In the same blood samples, leptin, insulin, gastric inhibitory polypeptide (GIP), and prolactin decreased by 40-70%. On the first day of testing under extinction conditions-where the animals earned unexpected saline instead of cocaine-5-fold increases were seen for growth hormone and acetylated ghrelin and equal changes-in amplitude and latency-were seen in each of the other cases except for IGF-1 (which increased at a slower rate). Single-spike firing affects the tonic activation level of the dopamine system, involving very different controls than those that drive burst firing; thus, the present data suggest interesting new targets for medications that might be used in the early stages of drug abstinence.
MeSH term(s)	Adiponectin/blood ; Animals ; Cocaine/administration & dosage ; Cocaine/pharmacology ; Cocaine-Related Disorders/blood ; Corticosterone/blood ; Disease Models, Animal ; Drug Substitution/methods ; Gastric Inhibitory Polypeptide/blood ; Ghrelin/blood ; Glucagon-Like Peptide 1/blood ; Growth Hormone/blood ; Injections, Intravenous ; Insulin/blood ; Leptin/blood ; Prolactin/blood ; Rats ; Reward ; Saline Solution/administration & dosage ; Saline Solution/pharmacology ; Self Administration ; Signal Transduction/drug effects
Chemical Substances	Adiponectin ; Adipoq protein, rat ; Ghrelin ; Insulin ; Leptin ; Saline Solution ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1) ; Prolactin (9002-62-4) ; Growth Hormone (9002-72-6) ; Cocaine (I5Y540LHVR) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2018-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	191042-5
ISSN	1873-5177 ; 0091-3057
ISSN (online)	1873-5177
ISSN	0091-3057
DOI	10.1016/j.pbb.2018.11.001
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