Penny Riha

Penny Riha, Ph.D

Penny Riha, Ph.D

pdriha@gmail.com
Senior Laboratory & Project Manager

I became interested in neurological research during my undergraduate studies at UT Austin.  After graduating with a BA in Psychology, I decided to attend graduate school at UT Austin with a major focus in Behavioral Neuroscience and supporting work in Toxicology.  I was interested in both normal brain aging and neurodegeneration.  I decided to study under Dr. Gonzalez-Lima due to his expertise in metabolic brain imaging and his unique perspective of the mitochondrial cause of Alzheimer’s disease.  I began my graduate studies examining behavior and brain effects of metabolic-enhancing drugs on learning and memory in both young and aged rats.  For my dissertation, I independently created a unique rodent model of early-stage Alzheimer’s disease called mild cognitive impairment.  After earning my Ph.D. in 2007, I decided to learn more about molecular aspects of disease and aging, and worked as a postdoctoral fellow under Dr. Michelle A. Lane in the Division of Nutritional Sciences at UT Austin.  I studied the chemotherapeutic mechanisms of retinoids in colorectal cancer cell lines.  Learning techniques ranging from RNA assays to transfection allowed me to appreciate the molecular mechanisms underlying disease.

After finishing my postdoctoral position, I began working in June 2009 in the Laboratory of Dr. Andrea Gore within the Division of Pharmacology & Toxicology.  One major focus in the laboratory is studying reproductive function and the primary regulator, gonadotropin-releasing hormone (GnRH).  GnRH is released in the median eminence, and as such, is a major area of interest.  In addition to my role as Senior Laboratory Manager, I also manage projects that include characterizing the hypothalamic changes in ovariectomized rats receiving hormone replacement therapy.  Specifically, we are testing the hypothesis that there are critical windows of opportunity and durations of hormone treatment that will affect hypothalamic circuits regulating reproduction in aging female rats.  Another major project is based on the hypothesis that glutamate is critical in normal reproductive function and may mediate the transition to acyclicity at middle age.  We are testing the effects of chronic glutamatergic NMDA receptor agonists and antagonists on reproductive behavior and hypothalamic function.  In both projects, we are measuring steroid hormone levels using radioimmunoassays as well as quantitating membrane receptor changes using both light and confocal microscopy.  In addition, we are using electron microscopy to describe qualitative changes in the synaptic ultrastructure of the median eminence, including neural-glial relationships.

Studying the neural mechanisms of reproductive development and aging was a natural transition from my graduate studies.  Working in the Gore Lab has allowed me to use my existing skills as well as expand my skill set in the laboratory.  I feel fortunate to work in a lab that values teamwork and encourages innovative ideas.

Peer-Reviewed Publications

Riha PD, Rojas JC, Colorado RA, & Gonzalez-Lima F. (2008).  Animal model of posterior cingulate cortex hypometabolism implicated in amnestic MCI and AD.  Neurobiology of Learning and  Memory, 90, 112-124.

Wrubel KM, Riha PD, Maldonado, MA, McCollum D, & Gonzalez-Lima F. (2007).  The brain metabolic enhancer methylene blue improves discrimination learning in rats.  Pharmacology, Biochemistry & Behavior, 86(4), 712-717.

Riha PD, Bruchey AK, Echevarria DJ, & Gonzalez-Lima F. (2005). Memory facilitation by methylene blue: dose-dependent effect on behavior and brain oxygen consumption. European Journal of Pharmacology, 511, 151-158.

Callaway NL, Riha PD, Bruchey AK, Munshi Z, & Gonzalez-Lima F. (2004). Methylene blue improves brain oxidative metabolism and memory retention in rats. Pharmacology, Biochemistry and Behavior, 77, 175-181.

Callaway NL, Riha PD, Wrubel KM, McCollum D, & Gonzalez-Lima F. (2002). Methylene blue restores spatial memory retention impaired by an inhibitor of cytochrome oxidase in rats. Neuroscience Letters, 332, 83-86.