Anatomy of Motivation

Watts, Alan G.; Swanson, Larry W.

doi:10.1002/0471214426.pas0314

Cited by 15 publications

(17 citation statements)

References 261 publications

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“…Diverse information about rewards is funneled through pathways from the nucleus accumbens (NAc) to the ventral pallidum (VP) embedded in larger mesocorticolimbic circuitry (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). Food, sex, drugs, winning money, and other rewards or predictive cues all activate these pathways in humans and other animals (11,(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29).…”

mentioning

confidence: 99%

“…Recent evidence indicates a surprising multiplicity of control systems within the NAc and VP, including multiple parallel and segregated loops that carry point to point signals through restricted subregions of prefrontal cortex-NAc-VP-thalamus and back again (7). Modulation by diverse neurochemicals also contributes to mediating separable hedonic and motivation functions (1,10,25,30,31).…”

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confidence: 99%

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Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Smith

Berridge

Aldridge

2011

Proc. Natl. Acad. Sci. U.S.A.

354

330

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Multiple signals for reward-hedonic impact, motivation, and learned associative prediction-are funneled through brain mesocorticolimbic circuits involving the nucleus accumbens and ventral pallidum. Here, we show how the hedonic "liking" and motivation "wanting" signals for a sweet reward are distinctly modulated and tracked in this circuit separately from signals for Pavlovian predictions (learning). Animals first learned to associate a fixed sequence of Pavlovian cues with sucrose reward. Subsequent intraaccumbens microinjections of an opioid-stimulating drug increased the hedonic liking impact of sucrose in behavior and firing signals of ventral pallidum neurons, and likewise, they increased incentive salience signals in firing to the reward-proximal incentive cue (but did not alter firing signals to the learned prediction value of a reward-distal cue). Microinjection of a dopamine-stimulating drug instead enhanced only the motivation component but did not alter hedonic impact or learned prediction signals. Different dedicated neuronal subpopulations in the ventral pallidum tracked signal enhancements for hedonic impact vs. incentive salience, and a faster firing pattern also distinguished incentive signals from slower hedonic signals, even for a third overlapping population. These results reveal separate neural representations of wanting, liking, and prediction components of the same reward within the nucleus accumbens to ventral pallidum segment of mesocorticolimbic circuitry.addiction | obesity | limbic | reinforcement | striatum

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mentioning

confidence: 99%

mentioning

confidence: 99%

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Smith

Berridge

Aldridge

2011

Proc. Natl. Acad. Sci. U.S.A.

354

330

View full text Add to dashboard Cite

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“…Instead they operate collectively by sculpting the function of large complex neural networks. The outputs of these networks are integrated with other brain processes to drive those motor functions that are dysregulated in T2D, including feeding, sympathoadrenal and pancreatic hormone release, and liver and adipose tissue function [16-18]. So to understand how the brain functions during T2D we need to know in some detail how these brain networks are structurally and functionally organized: basically, how is the brain wired for T2D?…”

Section: Brain Wiring and Metabolic Functionmentioning

confidence: 99%

“…However, organizational models based on single discrete “control centers” in the brain for feeding and other motivated behaviors have long been discredited. They have been replaced by the notion of distributed neural networks that encompass many brain regions to coordinate all the behavioral, autonomic, and endocrine motor components associated with a particular behavior, including metabolic control [16,52,53]. …”

Section: The Conundrum Of the Ventromedial Nucleus Of The Hypothalamumentioning

confidence: 99%

How Do We Know if the Brain Is Wired for Type 2 Diabetes?

Watts

2014

Curr Diab Rep

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It is now widely accepted that the brain makes important contributions to the dysregulated glucose metabolism, altered feeding behaviors, and the obesity often seen in type 2 diabetes (T2D). Although studies focusing on genetic, cellular, and molecular regulatory elements in pancreas, liver, adipose tissue etc. provide a good understanding of how these process relate to T2D, our knowledge of how brain wiring patterns are organized is much less developed. This article discusses animal studies that illustrate the importance of understanding the network organization of those brain regions most closely implicated in T2D. It will describe the brain networks, as well as the methodologies used to explore them. To illustrate some of the gaps in our knowledge, we will discuss the connectional network of the ventromedial nucleus and its adjacent cell groups in the hypothalamus; structures that are widely recognized as key elements in the brain’s ability to control glycemia, feeding, and body weight.

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“…In the 1960s, those other structures were sometimes thought of as part of the greater lateral hypothalamus area but today the anterior-lateral region of ventral forebrain is recognized to contain several distinct structures with their own distinctive neuronal compositions, circuitry connections, and functions. These outside regions include the ventral pallidum, which is in front and immediately adjacent to the lateral hypothalamus, the basal nucleus (which is often spoken of in connection with acetylcholine projections to the neocortex) and the sublenticular extended amygdala (part of the larger extended amygdala complex that also includes the central and medial nuclei of the amygdala and the bed nucleus of the stria terminalis) [28,29,70,92]. …”

Section: Stages and Change Over Timementioning

confidence: 99%

Contributions of Philip Teitelbaum to affective neuroscience

Berridge

2012

Behavioural Brain Research

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As part of a festschrift issue for Philip Teitelbaum, I offer here the thesis that Teitelbaum deserves to be viewed as an important forefather to the contemporary field of affective neuroscience (which studies motivation, emotion and affect in the brain). Teitelbaum’s groundbreaking analyses of motivation deficits induced by lateral hypothalamic damage, of roles of food palatability in revealing residual function, and of recovery of ‘lost’ functions helped shape modern understanding of how motivation circuits operate within the brain. His redefinition of the minimum requirement for identifying motivation raised the conceptual bar for thinking about the topic among behavioral neuroscientists. His meticulous analyses of patterned stages induced by brain manipulations, life development and clinical disorders added new dimensions to our appreciation of how brain systems work. His steadfast highlighting of integrative functions and behavioral complexity helped provide a healthy functionalist counterbalance to reductionist trends in science of the late 20th century. In short, Philip Teitelbaum can be seen to have made remarkable contributions to several domains of psychology and neuroscience, including affective neuroscience.

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Anatomy of Motivation

Cited by 15 publications

References 261 publications

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

How Do We Know if the Brain Is Wired for Type 2 Diabetes?

Contributions of Philip Teitelbaum to affective neuroscience

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