Altered Reward Processing in Women Recovered From Anorexia Nervosa

Wagner, Angela; Aizenstein, Howard J.; Venkatraman, Vijay K.; Fudge, Julie L.; May, James C.; Mazurkewicz, Laura; Frank, Guido; Bailer, Ursula F.; Fischer, Lorie; Nguyen, Van Thu; Carter, Cameron; Putnam, Karen; Kaye, Walter H.

doi:10.1176/appi.ajp.2007.07040575

Cited by 303 publications

(282 citation statements)

References 38 publications

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“…Functional MRI studies using disorder-relevant stimuli such as high calorie foods and distorted body images induce elevated amygdala reactivity in subjects with AN relative to healthy controls (Ellison et al, 1998;Joos et al, 2011); positron emission tomography studies show hypoperfusion of structures associated with fear extinction-namely the medial prefrontal cortex-and hyperperfusion of the amygdala À hippocampal complex in AN (Takano et al, 2001). Consistent with this clinical perspective, our results suggest that CR may normalize dysregulated fear responses in AN, which in combination with trait or acquired alterations in cortico-striatal circuit function that have been described in AN, may help explain why dieting behavior is so vigorously reinforced as well as the high comorbidity of anorexia with obsessive-compulsive disorder (Milad and Rauch, 2012;Wagner et al, 2007;Zheng et al, 2012).…”

Section: Discussionsupporting

confidence: 81%

Caloric Restriction Enhances Fear Extinction Learning in Mice

Riddle

McKenna

Yoon

et al. 2013

Neuropsychopharmacol

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Fear extinction learning, the ability to reassess a learned cue of danger as safe when it no longer predicts aversive events, is often dysregulated in anxiety disorders. Selective serotonin reuptake inhibitors (SSRI's) enhance neural plasticity and their ability to enhance fear extinction learning may explain their anxiolytic properties. Caloric restriction (CR) has SSRI-like effects on neural plasticity and anxiety-related behavior. We implemented CR in mice to determine its effects on conditioned-fear responses. Wild type and serotonin transporter (SERT) knockout mice underwent CR for 7 days leading to significant weight loss. Mice were then tested for cued fear learning and anxiety-related behavior. CR markedly enhanced fear extinction learning and its retention in adolescent female mice, and adults of both sexes. These effects of CR were absent in SERT knockout mice. Moreover, CR phenocopied behavioral and molecular effects of chronic fluoxetine, but there was no additive effect of CR in fluoxetine-treated mice. These results demonstrate that CR enhances fear extinction learning through a SERT-dependent mechanism. These results may have implications for eating disorders such as anorexia nervosa (AN), in which there is a high prevalence of anxiety before the onset of dietary restriction and support proposals that in AN, CR is a motivated effort to control dysregulated fear responses and elevated anxiety.

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Section: Discussionsupporting

confidence: 81%

Caloric Restriction Enhances Fear Extinction Learning in Mice

Riddle

McKenna

Yoon

et al. 2013

Neuropsychopharmacol

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“…Wagner and colleagues [341] reported increased CN activation to monetary-reward outcomes in women recovered from anorexia, and relatively equivalent CN responses to monetary gains and losses (a strongly similar pattern of results to that found by Wagner et al . in bulimia in [323]), suggesting possible similarities in reward-circuitry response in AN and bulimia.…”

Section: Reviewsupporting

confidence: 73%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

253

207

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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“…For instance, in previous AN brain-imaging studies, AN individuals were more responsive than controls to images of thin bodies in the ventral striatum, a dopamine and rewardrelated brain region (Fladung et al, 2010). Recovered AN showed reduced brain response to repeated application of sweet taste in the insula and striatum (Wagner et al, 2008), but increased response in the caudate nucleus to randomly given monetary (Wagner et al, 2007) or taste reward stimuli (Cowdrey et al, 2011). Overall, the brain-imaging literature on brain reward function in AN indicates brain reward system alterations in that disorder.…”

Section: Introductionmentioning

confidence: 93%

Anorexia Nervosa and Obesity are Associated with Opposite Brain Reward Response

Frank

Reynolds

Shott

et al. 2012

Neuropsychopharmacol

279

257

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Anorexia nervosa (AN) is a severe psychiatric disorder associated with food avoidance and malnutrition. In this study, we wanted to test whether we would find brain reward alterations in AN, compared with individuals with normal or increased body weight. We studied 21 underweight, restricting-type AN (age M 22.5, SD 5.8 years), 19 obese (age M 27.1, SD 6.7 years), and 23 healthy control women (age M 24.8, SD 5.6 years), using blood oxygen level-dependent functional magnetic resonance brain imaging together with a rewardconditioning task. This paradigm involves learning the association between conditioned visual stimuli and unconditioned taste stimuli, as well as the unexpected violation of those learned associations. The task has been associated with activation of brain dopamine reward circuits, and it allows the comparison of actual brain response with expected brain activation based on established neuronal models. A group-by-task condition analysis (family-wise-error-corrected Po0.05) indicated that the orbitofrontal cortex differentiated all three groups. The dopamine model reward-learning signal distinguished groups in the anteroventral striatum, insula, and prefrontal cortex (Po0.001, 25 voxel cluster threshold), with brain responses that were greater in the AN group, but lesser in the obese group, compared with controls. These results suggest that brain reward circuits are more responsive to food stimuli in AN, but less responsive in obese women. The mechanism for this association is uncertain, but these brain reward response patterns could be biomarkers for the respective weight state.

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Altered Reward Processing in Women Recovered From Anorexia Nervosa

Cited by 303 publications

References 38 publications

Caloric Restriction Enhances Fear Extinction Learning in Mice

Caloric Restriction Enhances Fear Extinction Learning in Mice

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Anorexia Nervosa and Obesity are Associated with Opposite Brain Reward Response

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