Haley Mendoza-Romero Email and Phone Number

My project is focused on how microglia interact with neural circuits in the hypothalamus during postnatal development. Microglia are the resident immune cells of the central nervous system and are known to be active regulators of development. However, there has not yet been a proposed role for microglia in the development of hypothalamic feeding circuits. The premise of my dissertation research is that maternal high fat diet during lactation (MHFD-L) causes a regionally specific activation of microglia that perturbs the organization of hypothalamic feeding circuits, associated with permanent disruption of metabolic phenotype in the offspring. I am currently working to establish how MHFD-L affects microglial participation in the development of hypothalamic feeding circuitry during the postnatal period. Additionally, I plan to determine if microglial phagocytosis in MHFD-L offspring contributes to disruption in hypothalamic feeding circuits. Completion of these goals will establish a novel framework for understanding how microglia contribute to the development of hypothalamic feeding circuits and potentially permanently influence metabolic phenotype. Mentor: Richard Simerly, Ph.D.

The first year, I focused on using in situ hybridization for the examination and characterization of hypothalamic pathology as a result of prenatal alcohol exposure. Molecular markers previously identified by Shimigori et al. were used as indicators of specific nuclei, with particular interest in the PVH and ARH. Specimens were selected and assessed based on a previously identified range of facial and ocular anomalies that indicate various stages on the spectrum of Fetal Alcohol Spectrum Disorder (FASD) or holoprosencephaly. Mentor: Kathleen Sulik, Ph.D.The second year, I focused on studying BAX (bcl-2-like protein 4), a pro-apoptotic protein to determine if subsequent cell death as a result of prenatal ethanol exposure plays a role in mediating craniofacial teratogenesis. The Sonic Hedgehog (Shh) signalling pathway is involved in the formation of craniofacial abnormalities associated with prenatal alcohol exposure, but it is unknown whether Shh signaling alterations are the immediate cause or if apoptosis is the key to understanding susceptibility. Mentor: Scott Parnell, Ph.D.

I worked on developing a method of assessment of dose-dependent ethanol toxicity in Zebrafish through behavioral trials. A Conditioned Place Preference (CPP) assay was created to determine environmental preference based on location of ethanol exposure. PI: Edward Levin, Ph.D.

Study focused on the efficacy of an integrative health coaching treatment program for Tinnitus.

Clerical duties, including data entry and resource management. Managed a project that converted education manuscripts and student files into an electronic database. Created an archive that detailed the contents of several files and helped faculty more easily access vital documents.

Called on behalf of the Duke Annual Fund to raise money for Student Financial Aid and other organizations on campus. Interacted with a broad range of alumni in a friendly, positive manner over the phone.