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Behavioural characteristics of the Prader-Willi syndrome related biallelic Snord116 mouse model
Jerzy Zieba1, Jac Kee Low2, Louise Purtell3
1Neuroscience Research Australia, Randwick, NSW 2031, Australia; Schizophrenia Research Institute, Darlinghurst, NSW 2010, Australia.
Insights
Mice lacking the Snord116 gene show altered locomotion and anxiety, but normal sociability and memory. This Prader-Willi syndrome (PWS) model offers insights into the genetic basis of PWS behaviors.
Area of Science:
- Genetics
- Neuroscience
- Behavioral Science
Background:
- Prader-Willi syndrome (PWS) is a genetic disorder causing obesity and behavioral issues.
- The Snord116 gene is linked to PWS, but its role in behavior is unclear.
Purpose of the Study:
- To investigate the behavioral impact of Snord116 gene deficiency.
- To assess the relevance of Snord116 deficiency in mice as a model for PWS.
Main Methods:
- Generated mice lacking Snord116 on both alleles.
- Assessed motor behavior, exploration, locomotion, anxiety, sociability, social recognition memory, spatial working memory, and fear behaviors.
- Examined sex-specific effects.
Main Results:
- Mice lacking Snord116 showed normal motor behavior and exploration.
- Task-dependent alterations in locomotion and anxiety-related behaviors were observed.
- Sociability, social recognition memory, spatial working memory, and fear behaviors were unaffected. No sex-specific effects were found.
Conclusions:
- Biallelic Snord116 deficiency in mice results in specific endophenotypes.
- This mouse model shows partial face validity for Prader-Willi syndrome behaviors.
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.
