M.S. Research Mentors

Associate Professor, Pharmacology and Physiology
Ahern Lab
Office: Med-Dent SW401
Lab: Med-Dent SW402
Education: BSc (Hons), 1990, LL. B., 1991, University of Canterbury NZ, PhD 1996 (Australian National University)
Current Research: How do cells detect changes in the external or extracellular environment? We are interested in the fundamental mechanisms that allow cells to sense diverse chemical or physical stimuli. Our focus is a class of membrane ion channels called “Transient Receptor Potential” (TRP) channels. We also explore novel ligand signaling at G-protein coupled receptors both in neurons and immune cells. We use a combination of electrophysiological, cell imaging, genetic and biochemical techniques, and where possible, appropriate animal models.

Tinatin I. Brelidze

Assistant Professor, Pharmacology and Physiology
Brelidze Lab
(202) 687-6178
Office: Med-Dent SE406
Lab: Med-Dent SE406
Education: Diploma in Physics (Hons), Tbilisi State University (Georgia), 1996; Ph.D. Physiology & Biophysics, University of Miami, 2003
Current Research: Ion channels are integral membrane proteins that regulate the passage of ions through cell membranes.  Ion channels are essential for physiological function of living cells and abnormalities in ion channel function or expression pattern are often linked to inherited or acquired diseases. The research in my laboratory is focused on studies of mechanisms responsible for opening and closing of ion channels, identification of novel ion channel regulators and investigation of therapeutic potential of ion channel regulators.  In our studies we use a variety of methods, including electrophysiology, biochemistry techniques, fluorescence-based methods, and zebrafish and rodent animal models.

Ghazaul Dezfuli

Assistant Professor, Pharmacology and Physiology
(202) 687-1091
Office: Med-Dent NW407
Lab: Med-Dent NW409, NW411
Education: Ph.D. (Neuroscience) Georgetown University, 2014
Current Research: My research focuses on how nicotine and selective nicotinic like drugs cause weight loss. Specifically, I am interested in understanding the critical role of nicotinic receptor desensitization in body weight regulation. Animal models of obesity, selective nicotinic-like drugs (agonists and antagonists), in vivo drug administration protocols, metabolic phenotyping, as well as more recently radioligand binding assays are used. The aim of this research is to apply our understanding of how nicotine is able to lower body weight and suppress food intake toward development of nicotine-based therapeutics for weight loss.

Patrick A. Forcelli

Assistant Professor, Pharmacology & Physiology
Website (new window)
Office: NRB W214
Education: Ph.D. (Neuroscience), Georgetown University, 2011
Current Research:  Research in the laboratory focuses on the neural circuitry underlying seizure propagation, complex behaviors, and the pharmacological treatment of neonatal seizures. We use a combination of approaches ranging from biochemistry and histology to neurophysiology (in slice and in intact animals) to behavioral monitoring and circuit manipulation (pharmacological, optogenetic, chemogenetic) to neuroimaging.

Adriane Fugh-Berman

Professor, Pharmacology & Physiology
Office: NRB W215
Education: M.D., Georgetown University, 1988
Current Research: I direct PharmedOut (new window), a research and education project that promotes rational prescribing practices. I research industry marketing techniques and how they interact with the culture of medicine, and teach physicians, other health care providers, graduate and medical students about clinical trials and evidence-based prescribing. I also teach about the risks and benefits of botanical medicines and dietary supplements, and direct the Urban Herbs (new window)project, an ecologic gardening project with various demonstration gardens on the GUMC campus. With Dr. Tom Sherman, I co-direct a new track in Natural Products within the masters program in pharmacology. I also direct theUrban Herbs project on the Georgetown campus. This is a garden project illustrating many medicinal plants.

Nady Golestaneh

Associate Professor, Opthalmology, Neurology, & Biochemistry
PubMed search for publications (new window)
(202) 687-8324
Office: Med/Dent NE203
Current Research: My research focuses on age-related macular degeneration (AMD). AMD is a devastating neurodegenerative disease and the leading cause of blindness in the elderly. More than 11 million Americans over the age of 50 are affected by AMD, and with an aging population, this number is expected to double by 2050. My research program involves three complementary areas in AMD, 1) investigating the underlying mechanism of AMD using adult stem cells and In vitro disease modeling, 2) establishment of new animal models to study AMD and test novel drugs in vivo, and 3) investigating how aging mechanisms can induce retinal degeneration and AMD.

Ken Kellar

Professor, Pharmacology and Physiology
Lab Website
(202) 687-1032
Office: Medical Dental Bldg SE402
Lab: Medical Dental Bldg NE416-420
Education: Ph.D., Pharmacology, The Ohio State University, 1974
Current Research: My laboratory studies the subunit composition, pharmacological properties and regulation of neuronal nicotinic receptors. We are particularly interested in understanding the importance of desensitization of these receptors and the mechanisms by which chronic exposure to nicotine increases these receptors in brain.

Professor, Pharmacology
(202) 687-0224
Office: NRB, W209B
Lab: DCM
Education: BA, MA Charles University Prague, Czech Republic; Ph.D. (1986) Czechoslovak Academy Sciences, Prague, Czech Republic
Current Research: Neural substrates of social and emotional behavior; the role of the amygdala and orbitofrontal cortex in processing reward; medial temporal lobe structures (hippocampus, perirhinal cortex) and cognitive functions (object recognition and spatial memory); amygdala and midbrain (superior colliculus) interactions; autism, PTSD; reversible pharmacological manipulations of discrete brain structures, systemic drug effects.

Alexey Ostroumov

Assistant Professor, Pharmacology and Physiology
Website (new window)
PubMed search for publications (new window)
Office: W224A NRB
Education: PhD, International School for Advanced Studies (SISSA, Italy), 2010
Current Research: Our main goal is to understand the causal mechanisms, by which modifications in synaptic plasticity contribute to neural circuit remodeling and aberrant behaviors associated with neuropsychiatric disorders. To this end, we combine slice and in vivo neurophysiology with viral-genetic and behavioral approaches.

Daniel Pak

Professor, Pharmacology and Physiology
Molecular Neurobiology of Memory [mNeMe]
(202) 687-8750
Office: SW407 Med/Dent
Lab: SW406 Med/Dent
Education: Harvard University, B.A., 1991; University of California at Berkeley, PhD, 1996
Current Research: My laboratory is interested in the molecular changes that occur at CNS synapses in response to experience. We utilize a combination of approaches ranging from molecular biology and biochemistry to cell biology, imaging, and mouse genetics to address three major questions: 1) how do neurons encode long-term storage of information? 2) how do neurons maintain stability of function by homeostatic synaptic plasticity mechanisms? and 3) how does failure of these mechanisms contribute to neurological and neurodegenerative disorders?

Niaz Sahibzada

Click for a complete list of published work in MyBiblography. (new window)

Professor, Division of Nephrology & Hypertension, Department of Medicine
Website (new window)
(202) 687-3010
Office: 232 Bldg D
Education: Ph.D. (Biochemistry), University of Maryland, 1987
Current Research: 1. Angiotensin receptor signaling and trafficking: The angiotensin type 1 receptor is a peptide hormone G protein-coupled receptor that is widely targeted to treat hypertension. We previously discovered that RNA binding proteins regulate the function of the rat type 1a receptor (AT1aR) by selectively binding within exon 2 of the receptor 5′-leader sequence and that this translational regulation is mediated by a short open reading frame in exon 2. More recently, this research direction has led to the exciting discovery of a seven amino acid peptide (PEP7) encoded within a short open reading frame in exon 2, which is a selective inhibitor of AT1aR signaling; PEP7 inhibits the Erk1/2 but not the classic inositol trisphosphate pathway. PEP7 may also contribute to age-related impairments in urine-concentrating mechanisms and modulates AT1aR trafficking. We study AT1aR signal transduction by conducting enzyme and radioligand binding assays as well as by measuring signaling molecules on Western blots. AT1aR trafficking is investigated using live cell imaging and confocal microscopy in cells transfected with wildtype and site-directed mutants of the AT1aR.
2. Immune system and hypertension: Our laboratory investigates T cell mechanisms underlying the susceptibility and resilience to developing hypertension. We have found that male T cells exacerbate hypertension in an induced model of hypertension in the male mouse but are unable to achieve the same magnitude of hypertension in the female. Furthermore, female T cells are not able to contribute to hypertension in the male mouse. These findings indicate biological sex is a critical determinant in T cell differentiation and/or function. We are currently investigating how gonadal hormones and sex chromosomes affect sex-specific T cell function in models of hypertension and associated vascular and renal disease. We study blood pressure and heart rate by radiotelemetry in conscious mice and rats. T cell expression and function is assessed by flow cytometry and cytokine production in the Dahl rat model, gene-specific knockout mice and the four core genotype mouse model that enables separation of sex chromosomes from gonadal hormones.
3. Ovarian hormone loss, physical activity, blood pressure and cognition: Recent laboratory studies focus on the physical and cognitive effects of bilateral oophorectomy prior to the age of natural menopause. The resulting sudden ovarian hormone loss accelerates the age-associated development of hypertension and cognitive decline. We are also studying how physical activity and blood pressure can modulate cognitive decline in this model. Physical activity is controlled using voluntary and forced running wheels. Cognition is assessed by a 12 arm radial maze and novel object recognition tests. In addition, we are studying these questions through human subject research using wireless technology, home blood pressure, heart rate and pulse wave velocity monitors in conjunction with consumer activity trackers.

Nataliia V. Shults

Assistant Professor, Pharmacology & Physiology
(202) 687-9205
Office: NW404 Med/Dent
Lab: NW403 Med/Dent
Education: M.D. National Medical University, Kiev, Ukraine, 1997; Ph.D. National Medical Academy, Kiev, Ukraine, 2005
Current Research: My current research focus is to determine the mechanism of how the damaged heart can be repaired. I am interested in the ultrastructural changes and metabolic aspects in the myocardium, which are involved to the mechanisms of cardiac repair using histological, immunohistochemical, histochemical methods, scanning and transmission electron microscopy. I am searching for novel therapeutic approaches to cardiac regeneration.

Yuichiro Suzuki

Professor, Pharmacology & Physiology
Homepage (new window)
(202) 687-8090
Office: NW402a Med/Dent
Lab: NW403 Med/Dent
Education: PhD, Medical College of Virginia,1991
Current Research: The general goal of my laboratory is to investigate signal transduction mechanisms for cardiac and smooth muscle cell regulation in order to develop therapeutic strategies against various heart and lung diseases. I have a long-standing interest in how redox processes regulate cell signaling, and my laboratory continues to contribute to the understanding of the mechanism of redox signaling. Another major focus of my laboratory is to study mechanisms of cell growth and death in pulmonary vascular smooth muscle and right heart muscle. We seek to develop therapeutic strategies to treat pulmonary hypertension patients, without adversely affecting the weakened right heart.

Stefano Vicini

Professor, Pharmacology & Physiology
Vicini Lab Website
(202) 687-6441
Office: BSB, 225
Lab: BSB, 228-230
Education: Ph.D., U Torino, Italy, 1979
Current Research: Using transgenic mice with the two major striatal output pathways labeled we are answering a fundamental question: What role tonic and phasic GABA and NMDA conductance plays in striatal disorders? We are studying the functional consequence of the activation of distinct dopamine receptors on NMDA and GABAa receptor subtypes. Our study has great potential to identify novel therapeutic targets for treating disorders associated with striatal dysfunction including Parkinson’s disease, Huntington’s disease, tardive dyskinesia, Tourette’s syndrome and drug addiction.

Tingting Wang

Assistant Professor, Pharmacology & Physiology
Wang Lab Website
(202) 687-1099
Office: SE407 Med/Dent
Lab:  SE407 Med/Dent
Education: Ph.D., Neurobiology, Duke University, 2009
Current Research:  The brain is incredibly complex and malleable in terms of developmental and learning-related plasticity. Homeostatic signaling systems act to stabilize the function of individual nerve cells and neural circuitry, thereby ensuring robust and reproducible brain function and behavior throughout life. My laboratory investigates the molecular mechanisms that underlie the homeostatic control of the nervous system and studies how impaired homeostatic plasticity is involved in neurological, neuropsychiatric and neurodegenerative disorders. We are particularly interested in the intercellular signals that convey information between neurons and glia during homeostatic plasticity. We use an array of cutting-edge electrophysiological, imaging, molecular and genetic tools in Drosophila melanogaster and mice to address:
1. What is the signaling function of glia in synaptic homeostatic plasticity?
2. How does dynamic regulation of extracellular matrix (ECM) and adhesion molecules modulate synaptic transmission?
3. How do genetic mutations and failed homeostasis contribute to neurological and psychiatric diseases, such as epilepsy, autism spectrum disorders and Alzheimer’s Disease?

Robert P. Yasuda

Assistant Professor, Pharmacology & Physiology
Yasuda Lab
Office: Med-Dent SW407 
Lab: Med-Dent NE411
Education: University of Colorado, Ph.D. (Pharmacology) 1986
Current Research: My laboratory is involved in the study of the structure and function of neuronal nicotinic receptors in the brain that are composed of five protein subunits that act as ligand-gated ion channels. These receptors are thought to be involved in the ncotine addition seen in smokers. We utilize molecular biological, biochemical and electrophysiological methods to study these receptors. Specifically, we are interested in understanding the nature of the nicotine binding site and how the order of these nicotinic receptor subunits affects function. One approach we are currently using is the creation of concatamers of the nicotinic receptor subunits that allow us to make receptors composed of subunits of known order and composition.