Resume

• 2014

  Northern Michigan University

  Taught Human Physiology (BI 202)

  Human Anatomy and Physiology 1 and 2 (BI 207 and BI 208)

  Clinical Neuroscience (BI 495/595)

  Introductory Neuroscience (BI 295)

  Methods in Biological Research (BI 564)

  Northern Michigan University

  Assistant Professor

  Assistant Professor of teaching in the Neuroscience Program at Michigan State University.

  Michigan State University

  Post-Doctoral Research Associate

  University of Minnesota

  Neuroscience Ph.D student

  University of Minnesota

• 2008

  Doctor of Philosophy (Ph.D.)

  Neuroscience

  Society for Neuroscience

  Organization for the Study of Sex Differences

  Society for Behavioral Neuroendocrinology

  University of Minnesota-Twin Cities

• 2005

  Neuroscience

  Purdue University

• 2001

  Bachelor of Science (B.S.)

  Biology

  General

  Tri Beta

  John Carroll University

• Informed high school students about how to pursue a career in academia.

  South Washington County Schools

  Brain Awareness Week Teacher

  Visited 3rd

  4th

  and 5th grade classrooms and presented introductory neuroscience information and conducted fun classroom activities

  University of Minnesota Department of Neuroscience

  Presenter

  Volunteered to discuss how human brains and the brains of animals control sexual behavior and sexual reward to adults. Real brain specimens were used to show attendees specific anatomical structures.

  Science Museum of Minnesota

  Social Science: Chemistry of Love and the Science of Sex

  Laboratory

  Fluorescence Microscopy

  Cell Culture

  Research

  Neuroscience

  Immunohistochemistry

  Immunofluorescence

  University Teaching

  Data Analysis

  Behavioral Neuroscience

  Western Blotting

  Animal Models

  stereotaxic surgery

  real-time PCR

  Microscopy

  ovariectomy

  Biology

  Mammalian Cell Culture

  Palmitoylation of estrogen receptors is essential for neuronal membrane signaling.

  Paul Mermelstein

  Kyla Britson

  Krista Tuomela

  Britni Peterson

  In addition to activating nuclear estrogen receptor signaling

  17β-estradiol can also regulate neuronal function via surface membrane receptors. In various brain regions

  these actions are mediated by the direct association of estrogen receptors (ERs) activating metabotropic glutamate receptors (mGluRs). These ER/mGluR signaling partners are organized into discrete functional microdomains via caveolin proteins. A central question that remains concerns the underlying mechanism by which these subpopulations of ERs are targeted to the surface membrane. One candidate mechanism is S-palmitoylation

  a posttranscriptional modification that affects the subcellular distribution and function of the modified protein

  including promoting localization to membranes. Here we test for the role of palmitoylation and the necessity of specific palmitoylacyltransferase proteins in neuronal membrane ER action. In hippocampal neurons

  pharmacological inhibition of palmitoylation eliminated 17β-estradiol-mediated phosphorylation of cAMP response element-binding protein

  a process dependent on surface membrane ERs. In addition

  mutation of the palmitoylation site on estrogen receptor (ER) α blocks ERα-mediated cAMP response element-binding protein phosphorylation. Similar results were obtained after mutation of the palmitoylation site on ERβ. Importantly

  mutation of either ERα or ERβ did not affect the ability of the reciprocal ER to signal at the membrane. In contrast

  membrane ERα and ERβ signaling were both dependent on the expression of the palmitoylacyltransferase proteins DHHC-7 and DHHC-21. Neither mGluR activity nor caveolin or ER expression was affected by knockdown of DHHC-7 and DHHC-21. These data collectively suggest discrete mechanisms that regulate specific isoform or global membrane ER signaling in neurons separate from mGluR activity or nuclear ER function.

  Palmitoylation of estrogen receptors is essential for neuronal membrane signaling.

  Paul Mermelstein

  Jill Becker

  Christel Westenbroek

  Adam N Perry

  After reproductive senescence or gonadectomy

  changes occur in neural gene expression

  ultimately altering brain function. The endocrine mechanisms underlying these changes in gene expression beyond immediate hormone loss are poorly understood. To investigate this

  we measured changes in gene expression the dorsal striatum

  where 17β-estradiol modulates catecholamine signaling. In human caudate

  quantitative PCR determined a significant elevation in β1-adrenergic receptor (β1AR) expression in menopausal females when compared with similarly aged males. No differences were detected in β2-adrenergic and D1- and D2-dopamine receptor expression. Consistent with humans

  adult ovariectomized female rats exhibited a similar increase in β1AR expression when compared with gonadectomized males. No sex difference in β1AR expression was detected between intact adults

  prepubertal juveniles

  or adults gonadectomized before puberty

  indicating the necessity of pubertal development and adult ovariectomy. Additionally

  increased β1AR expression in adult ovariectomized females was not observed if animals were masculinized/defeminized with testosterone injections as neonates. To generate a model system for assessing functional impact

  increased β1AR expression was induced in female-derived cultured striatal neurons via exposure to and then removal of hormone-containing serum. Increased β1AR action on cAMP formation

  cAMP response element-binding protein phosphorylation and gene expression was observed. This up-regulation of β1AR action was eliminated with 17β-estradiol addition to the media

  directly implicating this hormone as a regulator of β1AR expression. Beyond having implications for the known sex differences in striatal function and pathologies

  these data collectively demonstrate that critical periods early in life and at puberty program adult gene responsiveness to hormone loss after gonadectomy and potentially reproductive senescence.

  Enhanced striatal β1-adrenergic receptor expression following hormone loss in adulthood is programmed by both early sexual differentiation and puberty: a study of humans and rats.

  Hedges

  University of Minnesota

  Michigan State University