Reduced astrocyte density underlying brain volume reduction in activity-based anorexia rats

Frintrop, Linda; Liesbrock, Johanna; Paulukat, Lisa; Johann, Sonja; Kas, Martien; Tolba, René; Heussen, Nicole; Neulen, Joseph; Konrad, Kerstin; Herpertz‐Dahlmann, Beate; Beyer, Cordian; Seitz, Jochen

doi:10.1080/15622975.2016.1273552

Cited by 52 publications

(55 citation statements)

References 55 publications

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“…Accordingly, animals with the largest inhibitory contacts ran the least during food access and had the most prominent FAA. 44 Overall cortex and corpus callosum volumes in the brains of ABA rats have also been shown to be reduced by 6% and 9%, respectively, 45 compared to controls, in line with grey and white matter reductions reported in acute AN. 46 The acute phase of ABA (ie the first 3 days) is also associated with a reduction in hippocampal cell proliferation 47 and ABA rats demonstrate alterations in dendritic branching 48 and maturation of hippocampal neurones, 49 cellular substrates that could contribute to the reduced hippocampal volumes seen in acutely ill AN patients.…”

Section: Brain Structure and Function In Abasupporting

confidence: 71%

A focus on reward in anorexia nervosa through the lens of the activity‐based anorexia rodent model

Foldi

Milton

Oldfield

2017

J Neuroendocrinology

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Patients suffering anorexia nervosa (AN) become anhedonic, unable or unwilling to derive normal pleasures and tend to avoid rewarding outcomes, most profoundly in food intake. The activity-based anorexia model recapitulates many of the pathophysiological and behavioural hallmarks of the human condition, including a reduction in food intake, excessive exercise, dramatic weight loss, loss of reproductive cycles, hypothermia and anhedonia, and therefore it allows investigation into the underlying neurobiology of anorexia nervosa. The use of this model has directed attention to disruptions in central reward neurocircuitry, which may contribute to disease susceptibility. The purpose of this review is to demonstrate the utility of this unique model to provide insight into the mechanisms of reward relevant to feeding and weight loss, which may ultimately help to unravel the neurobiology of anorexia nervosa and, in a broader sense, the foundation of reward-based feeding. K E Y W O R D Sactivity-based anorexia, animal models, anorexia nervosa, dopamine, mesolimbic reward pathways | ANOREXIA NERVOSA AS A NEUROBIOLOGICAL DISORDERAnorexia nervosa (AN) is a debilitating psychiatric disorder of complex aetiology that is characterised by a relentless pursuit of weight loss through extreme food restriction and excessive exercise, as well as high rates of chronicity, morbidity and mortality.1 AN is accompanied by physiological, biochemical and behavioural disturbances, including a diminished capacity to experience pleasure or reward. Figure 1A). A core aspect of this hypothesis is that "top-down" cognitive modulatory mechanisms exert control over "bottom-up" ap- | NEUROCIRCUITRY MODULATING REWARD AND INHIBITIONIt is likely that AN behaviours are encoded in limbic and cognitive circuits that fall into two categories. The first may be described as "limbic" and involves the amygdala and ventral striatum, as well as regions of the cerebral cortex, including the insula, anterior cingulate and prefrontal regions, which collectively coordinate the affective response to stimuli including food and feeding. The current terminology introduced by Berridge and Kringelbach 11 is that "liking" is the actual pleasure component of reward and "wanting" is the measure of motivation or incentive salience for a reward. The microstructure of neural circuits and transmitters coding for pleasure can be subdivided, in simplistic terms, into (i) those dopaminergic projections originating in the ventral tegmental area (VTA) and extending to the nucleus accumbens (NAc) which account for "wanting" and (ii) the activation of μ-opioid, In addition to the interaction between these two broad determinants of anorexic behaviour, mesolimbic reward and cortical control, there are clearly modulatory influences form other regions that impinge on such circuits. One of these involves serotonin released from neurones originating in the midbrain raphe nuclei, which can influence reward processing and anhedonic behaviours via actions directly on the VTA, indire...

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Section: Brain Structure and Function In Abasupporting

confidence: 71%

A focus on reward in anorexia nervosa through the lens of the activity‐based anorexia rodent model

Foldi

Milton

Oldfield

2017

J Neuroendocrinology

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“…New studies detected astrocyte loss in both GM and WM of activity‐based anorexia rats after semi‐starvation. This could help explain neuronal dysfunctions leading to symptoms of rigidity and impaired learning in AN (Frintrop et al, ; Seitz, Konrad, & Herpertz‐Dahlmann, ).…”

Section: Discussionmentioning

confidence: 99%

“…Dehydration/rehydration and osmotic effects are believed to be unlikely to produce brain volume alterations of such extent (Bernardoni et al, 2016;King et al, 2015;Yau et al, 2013). Seitz et al (2016) This could help explain neuronal dysfunctions leading to symptoms of rigidity and impaired learning in AN (Frintrop et al, 2018;Seitz, Konrad, & Herpertz-Dahlmann, 2017).…”

Section: Global Segment Volumesmentioning

confidence: 99%

Recovery of cortical volume and thickness after remission from acute anorexia nervosa

Nickel

Joos

Elst

et al. 2018

Intl J Eating Disorders

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“…Atypical anorexia nervosa is defined as anorexia nervosa that does not meet full diagnostic criteria, typically those individuals are not below a certain weight threshold, such as the 5th percentile for age adjusted BMI. Two studies by Olivo et al found normal gray and white matter in adolescents with atypical anorexia nervosa, further supporting the hypothesis that body weight is directly related to brain structure, although the mechanism is not yet well understood (Frintrop et al, 2017;Olivo et al, 2018;Olivo et al, 2019).…”

Section: Research On Brain Structurementioning

confidence: 84%

Editorial to the virtual issue highlighting neuroscience based research in eating disorders to mark the 49th Society for Neuroscience Annual Meeting

Frank

2019

Intl J Eating Disorders

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Objective This virtual issue of the International Journal of Eating Disorders highlights recently published research that is based on neuroscience concepts, to mark the 49th Society for Neuroscience Annual Meeting in Chicago, IL, in November 2019. Methods and Results The collection of articles includes research published between 2018 and 2019 that fall within the broader field of clinical neuroscience. Those articles span a broad range of themes, including food intake regulation and reward circuitry, taste perception, decision‐making, cognitive and emotional bias, and targeting altered brain circuits using novel therapeutic methods. Discussion The eating disorders field as a whole is increasingly incorporating neuroscience‐based concepts when studying those disorders and developing disease models. We hope that this virtual issue will further stimulate discussion and research that is focused on brain circuits and neurobiology to study etiology and pathophysiology of eating disorders to develop more effective treatments.

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Reduced astrocyte density underlying brain volume reduction in activity-based anorexia rats

Cited by 52 publications

References 55 publications

A focus on reward in anorexia nervosa through the lens of the activity‐based anorexia rodent model

A focus on reward in anorexia nervosa through the lens of the activity‐based anorexia rodent model

Recovery of cortical volume and thickness after remission from acute anorexia nervosa

Editorial to the virtual issue highlighting neuroscience based research in eating disorders to mark the 49th Society for Neuroscience Annual Meeting

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