Binder, MarcShoenfeld, LIza2013-11-142013-11-142013-11-142013Shoenfeld_washington_0250O_12241.pdfhttp://hdl.handle.net/1773/24324Thesis (Master's)--University of Washington, 2013The loss of motoneurons is an undisputed feature of amyotrophic lateral sclerosis (ALS) and its animal models (SOD1 mutant mice), but how the disease affects the size and shape of motoneurons prior to their degeneration is less well understood. Some evidence suggests that presymptomatic changes in motoneuron size may be linked to an upregulation of the calcium-mediated persistent inward current (Ca-PIC) necessary for the bistability that characterizes motoneurons. To explore whether there is a correlation between increases in motoneuron size and the upregulation of the Cav1.3 channel responsible for the Ca-PIC, the present study employed a mutant G93A SOD1 mouse, the most widely used animal model for ALS. We found no detectable difference between soma area of motoneurons from mice transfected with the ALS mutant gene and its wild-type counterpart. Expression levels of the Cav1.3 calcium channel presented difficulties in analysis across image collection dates, but were not found to be differentiated by genotype, sex, or any interaction of the two. Interestingly, while analysis did not reveal an overall effect of sex on soma size, it did show an interaction effect between the male sex and SODG93A genotype, leading to a greater increase in soma area in males than in females. The implications of these findings, as well as procedural choices that may have limited the power and scope of this study, are discussed.application/pdfen-USCopyright is held by the individual authors.Neurosciencesbehavioral neuroscienceThesis