OBJECTIVES: The prevalence of autism in our society has grown over the past few decades while lack of a central pathophysiological cause for the disease has hindered research and design of an animal model with the disease. Methyl CpG Binding Domain-1 knockout mice are a potential model for autism. The mice are owned soley by Dr. Xinyu Zhao of the University of New Mexico. The mice appear normal, both anatomically and developmentally, however, they exhibit behaviors that are often seen in autistic patients. While there are few specific physiological hallmarks of autism among patients, a few studies have noted increased levels of adrenocorticotropin hormone and lower plasma corticosterone, which these mice exhibit. The project aims to look at the central deregulation of corticosterone releasing factor-hypothalamic-pituitary-adrenal axis by comparing the presence of receptors for corticosterone releaseing factor-1 in the hippocampi of knock-out mice and wildtype. METHODS: Six knock out mice and 6 wild type mice were euthanized and the hippocampi removed and homogenized. A western blot was conducted to determine relative amounts of corticosterone releasing factor receptor-1 in wild-type and knock out mice. Amount of the secondary antibody was quantified using the Pierce Supersignal West Pico Chemiluminescent Kit. RESULTS: The knockout mice had significantly less expression of corticosterone releasing factor receptor-1 in the hippocampi than wildtype p<0.03 CONCLUSIONS: The findings show that there is a difference in the central regulation of the corticosterone releasing factor-hypothalamic pituitary adrenal axis between wildtype and Methyl CpG Binding Domain-1 knockout mice. While additional studies are needed to understand the full-picture of the regulation of this axis in these mice, the project is promising in supporting the use of the methyl CpG Binding Domain-1 knockout mice as models to study the specific physiology of autism.
Heise, Laura and Andrea Allan. "Supporting the Use of MBD-1 Knockout Mice as an Animal Model for Autism." (2009). http://digitalrepository.unm.edu/ume-research-papers/66