ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2017
The Role of Mesolimbic Reward Neurocircuitry in Prevention and Rescue of the Activity-Based Anorexia (ABA) Phenotype in Rats.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Activity Based Anorexia as an Animal Model for Anorexia Nervosa-A Systematic Review.Frontiers in nutrition · 2019Pooled it
- A pontomesencephalic-mesolimbic circuit modulates activity-based anorexia.Science advances · 2026Article
- Leptin Reduces Running in a Rodent Anorexia Nervosa Model via a Distributed Neural Network.European eating disorders review : the journal of the Eating Disorders Association · 2026Article
- Neural circuits regulating activity-based anorexia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Activity-based anorexia enhances glutamatergic synaptic transmission and neuronal excitability within the nucleus accumbens of female mice.Physiological reports · 2026Article
- Comprehensive insights into emerging advances in the Neurobiology of anorexia.Journal of advanced research · 2026Review
- Cariprazine as a candidate for drug repurposing in anorexia nervosa: a mechanistic hypothesis grounded in neuroimaging evidence.Frontiers in pharmacology · 2026Article
- Reduced Ventral Tegmental Area GABA neuron output contributes to hyperactivity in the activity-based anorexia model in female mice.Nature communications · 2025Article
- Toward a Genetic Signature of Resistance to Activity-Based Anorexia in Striatal Projecting Cortical Neurons.The International journal of eating disorders · 2025Article
- High-fat diet-induced anorexia in rats: involving orosensory deficits, gastrointestinal dysfunction, intestinal taste receptor downregulation and dopamine signaling dysregulation.European journal of medical research · 2025Article
- Examining the biological causes of eating disorders to inform treatment strategies.Nature reviews. Neuroscience · 2025Review
- Endogenous opioid receptors and the feast or famine of maladaptive feeding.Nature communications · 2025Review
- Chemogenetic Tools and their Use in Studies of Neuropsychiatric Disorders.Physiological research · 2024Review
- A transdiagnostic and translational framework for delineating the neuronal mechanisms of compulsive exercise in anorexia nervosa.The International journal of eating disorders · 2024Review
- Development of activity-based anorexia requires PKC-δ neurons in two central extended amygdala nuclei.Cell reports · 2024Article
- Adaptive and Maladaptive Exercise in Eating Disorders.Current topics in behavioral neurosciences · 2024Review
- Article
- AgRP neurons coordinate the mitigation of activity-based anorexia.Molecular psychiatry · 2023Article
- GABAergic interneurons' feedback inhibition of dorsal raphe-projecting pyramidal neurons of the medial prefrontal cortex suppresses feeding of adolescent female mice undergoing activity-based anorexia.Brain structure & function · 2022Article
- A Framework for Developing Translationally Relevant Animal Models of Stress-Induced Changes in Eating Behavior.Biological psychiatry · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients suffering from anorexia nervosa (AN) become anhedonic; unable or unwilling to derive normal pleasures and avoid rewarding outcomes, most profoundly in food intake. The activity-based anorexia (ABA) model recapitulates many of the characteristics of the human condition, including anhedonia, and allows investigation of the underlying neurobiology of AN. The potential for increased neuronal activity in reward/hedonic circuits to prevent and rescue weight loss is investigated in this model. The mesolimbic pathway extending from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) was activated using a dual viral strategy, involving retrograde transport of Cre (CAV-2-Cre) to the VTA and coincident injection of DREADD receptors (AAV-hSyn-DIO-hM3D(Gq)-mCherry). Systemic clozapine-n-oxide (CNO; 0.3 mg/kg) successfully recruited a large proportion of the VTA-NAc dopaminergic projections, with activity evidenced by colocalization with elevated levels of Fos protein. The effects of reward circuit activation on energy balance and predicted survival was investigated in female Sprague-Dawley rats, where free access to running wheels was paired with time-limited (90 min) access to food, a paradigm (ABA) which will cause anorexia and death if unchecked. Excitation of the reward pathway substantially increased food intake and food anticipatory activity (FAA) to prevent ABA-associated weight loss, while overall locomotor activity was unchanged. Similar activation of reward circuitry, delayed until establishment of the ABA phenotype, rescued rats from their precipitous weight loss. Although these data are consistent with shifts primarily in food intake, the contribution of mechanisms including energy expenditure to survival remains to be determined. These results will inform the neurobiological underpinnings of AN, and provide insight into the mechanisms of reward circuitry relevant to feeding and weight loss.
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