ArticleThe European journal of neuroscience2015
Calorie seeking, but not hedonic response, contributes to hyperphagia in a mouse model for Prader-Willi syndrome.
Article in The European journal of neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Altered neural electrophysiological properties in the anterior cingulate cortex in a mouse model of Prader-Willi syndrome.The Journal of physiology · 2026Article
- The parenting hub of the hypothalamus is a focus of imprinted gene action.PLoS genetics · 2023Article
- Systematic investigation of imprinted gene expression and enrichment in the mouse brain explored at single-cell resolution.BMC genomics · 2022Article
- The contribution of imprinted genes to neurodevelopmental and neuropsychiatric disorders.Translational psychiatry · 2022Review
- Comparison of mouse models reveals a molecular distinction between psychotic illness in PWS and schizophrenia.Translational psychiatry · 2021Article
- A Comprehensive Review of Genetically Engineered Mouse Models for Prader-Willi Syndrome Research.International journal of molecular sciences · 2021Review
- Wistar Kyoto Rats Display Anhedonia In Consumption but Retain Some Sensitivity to the Anticipation of Palatable Solutions.Frontiers in behavioral neuroscience · 2020Article
- Prader-Willi syndrome imprinting centre deletion mice have impaired baseline and 5-HT2CR-mediated response inhibition.Human molecular genetics · 2019Article
- Preclinical Testing in Translational Animal Models of Prader-Willi Syndrome: Overview and Gap Analysis.Molecular therapy. Methods & clinical development · 2019Review
- Feeding behaviour, risk-sensitivity and response control: effects of 5-HTPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- Baby food and bedtime: Evidence for opposite phenotypes from different genetic and epigenetic alterations in Prader-Willi and Angelman syndromes.SAGE open medicine · 2019Review
- Article
- Paradoxical leanness in the imprinting-centre deletion mouse model for Prader-Willi syndrome.The Journal of endocrinology · 2017Article
- Behavioural abnormalities in a novel mouse model for Silver Russell Syndrome.Human molecular genetics · 2016Article
- Increased alternate splicing of Htr2c in a mouse model for Prader-Willi syndrome leads disruption of 5HTMolecular brain · 2016Article
- Article
- The origins of individual differences in how learning is expressed in rats: A general-process perspective.Journal of experimental psychology. Animal learning and cognition · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Prader-Willi syndrome (PWS) is a neurodevelopmental disorder caused by deletion or inactivation of paternally expressed imprinted genes on human chromosome 15q11-q13, the most recognised feature of which is hyperphagia. This is thought to arise as a consequence of abnormalities in both the physiological drive for food and the rewarding properties of food. Although a number of mouse models for PWS exist, the underlying variables dictating maladaptive feeding remain unknown. Here, feeding behaviour in a mouse model in which the imprinting centre (IC) of the syntenic PWS interval has been deleted (PWS(ICdel) mice) is characterised. It is demonstrated that PWS(ICdel) mice show hyperghrelinaemia and increased consumption of food both following overnight fasting and when made more palatable with sucrose. However, hyperphagia in PWS(ICdel) mice was not accompanied by any changes in reactivity to the hedonic properties of palatable food (sucrose or saccharin), as measured by lick-cluster size. Nevertheless, overall consumption by PWS(ICdel) mice for non-caloric saccharin in the licking test was significantly reduced. Combined with converging findings from a continuous reinforcement schedule, these data indicate that PWS(ICdel) mice show a marked heightened sensitivity to the calorific value of food. Overall, these data indicate that any impact of the rewarding properties of food on the hyperphagia seen in PWS(ICdel) mice is driven primarily by calorie content and is unlikely to involve hedonic processes. This has important implications for understanding the neural systems underlying the feeding phenotype of PWS and the contribution of imprinted genes to abnormal feeding behaviour more generally.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.