Bailey Kermath

Bailey Kermath

Bailey Kermath

baileykermath@gmail.com
PhD 2013, Institute for Neuroscience
Kermath CV (pdf)

Background: I graduated from the University of Wisconsin-Madison in 2006 with a B.S. in Biology; Neurobiology option. As an undergraduate, I worked in the laboratory of Dr. John G. White studying the role of the protein STU-10 in the rotation of mitotic spindle during asymmetric cell division in the C. elegans early embryo. Following my undergraduate studies, I volunteered as a research technician in Capulalpan de Mendez, Mexico for a Union de Comunidades Zapoteca-Chananteca (UZACHI) in their edible mushroom production lab and for Estudios Rulares y Asesora Campesina and Global Environmental Management (GEM) to test the local water quality. Next, I work as an analyst for Covance Laboratories before beginning the PhD program at UT-Austin in the Institute for Neuroscience in 2007. I first worked in the laboratories of Dr. Tim Schallert and F. Gonzalez-Lima investigating the neuroprotective effects of methylene blue in a rat model of Parkinson’s disease. I then joined Dr. Andrea Gore’s laboratory in the Dept. of Pharmacy to study hypothalamic mechanisms underlying the transition to menopause.

In addition to research at UT-Austin, I held offices in the Neuroscience Graduate Students’ Assocation (NGSA) and helped initiate and take part in Outreach activities to teach children K-8th grade about the brain. I also served as Chair of the student-run 15th Annual Neuroscience Symposium and TAed Comparative Animal Physiology, where I took part in “flipped classroom” instruction and problem-based group activities to facilitate interactive learning.

Dissertation Research: I joined the Gore Lab in the summer of 2009. My dissertation focused on hypothalamic changes underlying the transition to menopause using a novel ovarian-intact model of the natural progression to acyclicity in middle-aged female rats. In Aim 1, I demonstrated changes in expression of genes involved in sex steroid hormone feedback (receptors and steroidogenic enzymes) and excitatory neurotransmission (kisspeptin, other neuropeptides and neurotrophic factors) with reproductive aging within the arcuate nucleus (ARC) and median eminence (ME) of the hypothalamus. Cell counting of double-labeled immunofluorescent images confirmed a decrease in the percentage of kisspeptin neurons and their colocalization with estrogen receptor alpha in the ARC. Aim 2 results revealed the importance of glutamatergic signaling through the NMDA receptor in the ME in acyclicity, as chronic infusion of an antagonist for NR2b-containing NMDA receptors into the ME was able to partially restore aspects of reproductive physiology. Quantification of NR2b subunit protein expression through double-labeled immunofluorescence and correlation network analysis revealed the importance of the NR2b phosphorylation state and colocalization with GnRH terminals in the external zone of the ME in these processes. Lastly, in Aim 3 I showed, in collaboration with Dr. Deena Walker, gene expression changes in the ARC and ME with reproductive aging that were altered with perinatal endocrine disruption, including kisspeptin expression in the ARC and estrogen receptor alpha gene expression in the ME. Together my data suggest that the regulation of excitatory stimulation and hormone feedback at the site of GnRH processes and terminals are important hypothalamic mechanisms underlying the transition to acyclicity.