Stanford Summer Research Program (SSRP) 2008
This summer I had the opportunity of working at Dr. William Mobley’s lab by the mentorship of Dr. Ahmad Salehi at Stanford University. Here we study Down syndrome using a mouse model.
Norepinephrinergic System in Ts65Dn mouse model of Down Syndrome.
Jessenia Y. Laguna Torres1, 2, Ahmad Salehi2, William C. Mobley2
1Department of Biology, University of Puerto Rico, San Juan, Puerto Rico
2Department of Neurology & Neurological Sciences, Stanford University School of Medicine
Down Syndrome (DS) or trisomy 21 is a chromosomal disorder caused by the presence of all or part of an extra chromosome 21. The incidence of DS is estimated to be at 1 per 1,000 live births. Mental retardation is a common characteristic of all DS patients. As a model of DS, we use Ts65Dn mice trisomic for a segment of mouse chromosome 16, which contains many of the evolutionarily conserved genes of human chromosome 21. Previous data on the Ts65Dn mouse model of DS have shown that these mice are deficient in cognitive functions and undergo alterations in structures involved in cognition (e.g. the hippocampus). Norepinephrine (NE) is a neurotransmitter with a critical role in hippocampal functions. The sole source of NE for hippocampus is locus coeruleus. Our recent data indicate severe degeneration of LC neurons in Ts65Dn mice. We hypothesized that degeneration of LC in Ts65Dn mice would lead to decreased levels of NE and its receptors in the hippocampus. To investigate this, we performed immunohistochemistry on young adult (six-month-old) Ts65Dn mice and their age-matched controls using an antibody against b1-adrenergic receptors. We found a number of strongly stained interneurons in the dentate gyrus of the hippocampus. In addition, a large number of cortical neurons were stained. Currently, we are quantifying the total number and size of b1-positive-neurons in the dentate gyrus of Ts65Dn mice and controls using unbiased stereological methods. Our data would shed light on the question whether LC degeneration in Ts65Dn mice would affect b1-adrenergic receptor expression in the hippocampus and might suggest new therapies.
Poster Presentation
Oral Presentation
Summer Adventure
