Other Publications (1)
Articles by Abigail Lemons in JoVE
Noninvasive, High-throughput Determination of Sleep Duration in Rodents R. Michelle Saré1, Abigail Lemons1, Anita Torossian1, Carolyn Beebe Smith1 1Section on Neuroadaptation and Protein Metabolism, National Institute of Mental Health, National Institutes of Health We describe a high-throughput method of measuring sleep by means of activity-based home-cage monitoring. This method offers advantages over traditional EEG-based methods. It is well validated for the determination of total sleep duration and can be a powerful tool to monitor sleep in rodent models of human disease.
Other articles by Abigail Lemons on PubMed
Negative Effects of Chronic Rapamycin Treatment on Behavior in a Mouse Model of Fragile X Syndrome Frontiers in Molecular Neuroscience. | Pubmed ID: 29375310 Fragile X syndrome (FXS), the most common form of inherited intellectual disability, is also highly associated with autism spectrum disorders (ASD). It is caused by expansion of a CGG repeat sequence on the X chromosome resulting in silencing of the gene. This is modeled in the mouse by deletion of ( KO). KO mice recapitulate many of the behavioral features of the disorder including seizure susceptibility, hyperactivity, impaired social behavior, sleep problems, and learning and memory deficits. The mammalian target of rapamycin pathway (mTORC1) is upregulated in KO mice and is thought to be important for the pathogenesis of this disorder. We treated KO mice chronically with an mTORC1 inhibitor, rapamycin, to determine if rapamycin treatment could reverse behavioral phenotypes. We performed open field, zero maze, social behavior, sleep, passive avoidance, and audiogenic seizure testing. We found that pS6 was upregulated in KO mice and normalized by rapamycin treatment, but, except for an anxiogenic effect, it did not reverse any of the behavioral phenotypes examined. In fact, rapamycin treatment had an adverse effect on sleep and social behavior in both control and KO mice. These results suggest that targeting the mTOR pathway in FXS is not a good treatment strategy and that other pathways should be considered.