Abstract
Prader-Willi syndrome (PWS) is the predominant genetic cause of obesity in humans and is associated with several behavioural phenotypes such as altered motoric function, reduced activity, and learning disabilities. It can include mood instability and, in some cases, psychotic episodes. Recently, the Snord116 gene has been associated with the development of PWS, however, it's contribution to the behavioural aspects of the disease are unknown. Here we show that male and female mice lacking Snord116 on both alleles exhibit normal motor behaviours and exploration but do display task-dependent alterations to locomotion and anxiety-related behaviours. Sociability is well developed in Snord116 deficient mice as are social recognition memory, spatial working memory, and fear-associated behaviours. No sex-specific effects were found. In conclusion, the biallelic Snord116 deficiency mouse model exhibits particular endophenotypes with some relevance to PWS, suggesting partial face validity for the syndrome.
| Original language | English |
|---|---|
| Article number | 1658 |
| Pages (from-to) | 71-77 |
| Number of pages | 7 |
| Journal | Neuropeptides |
| Volume | 53 |
| DOIs | |
| Publication status | Published - Oct 2015 |
Bibliographical note
Publisher Copyright:© 2015 Elsevier Ltd.
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Prader-Willi syndrome
- anxiety
- behavior
- cognition
- mice
- proteins
- Social preference
- Behaviour
- SNORD116
- Cognition
- MBII-85
- HBII-85
- Anxiety
- Mouse model
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