MARGARET A. VIZZARD
Professor
Neurology and
Anatomy and Neurobiology
Ph.D., Thomas Jefferson University, 1992
Postdoctoral training, University of Pittsburgh
Bladder function is something that most of us take for granted. We assume that our daily trips to the bathroom and the occasional night-time visits will continue without problems. However, in the United States alone, an estimated 17 million individuals suffer from the effects of urinary bladder dysfunction. The main research focus in the Vizzard laboratory deals with the overactive bladder where increased frequency of voiding, urgency, incontinence and sometimes pain are the signs and symptoms. The cost of caring for the effects of urinary incontinence is no insignificant amount; in 1995, it was estimated at $25 billion per year. As the US population ages, the number of individuals suffering from overactive bladder will, without question, increase. It is also clear that a large number of clinical disorders resulting from diseases or injuries to the central nervous system involve urinary bladder dysfunction. Peripheral nerve injury, spinal cord injury, multiple sclerosis, stroke and interstitial cystitis are some of the many diseases or injuries that are associated with urinary bladder dysfunction. Thus, it is very important for the future treatment of many human illnesses that more detailed information is obtained about the organization of central and peripheral urinary bladder pathways. A better understanding of the mechanisms controlling the activities of the lower urinary tract would facilitate the diagnosis and treatment of these problems.
The Vizzard laboratory research interests concern the neural control, organization, electrical and neurochemical properties of urinary bladder and how these properties are altered following neural injury or disease. Current rodent models of bladder dysfunction include: spinal cord injury, peripheral nerve injury, acute and chronic bladder inflammation, and partial bladder outlet obstruction. The Vizzard laboratory defines the changes that occur with injury/disease and then determines what factors control and regulate these plastic changes. The Vizzard laboratory seeks to define interventional strategies that improve bladder function in the face of neural injury or disease. Below are some questions that frame the research activities in the Vizzard laboratory. Is the basic neural circuitry underlying bladder reflexes changed with disease/injury? What changes can account for shifting bladder reflex function into an overactive mode of operation? Are these changes reversible? What role does the urinary bladder, itself, play in altered bladder reflex function? Do neural changes and smooth muscle/urothelium changes both contribute to altered bladder function?
The Vizzard laboratory uses a multidisciplinary approach to address the above questions. Some of these techniques and approaches include: conventional and transneuronal tracing using neurotropic viruses (eg., pseudorabies virus and herpes simplex virus-type to map bladder reflex circuitry in health and disease; immunostaining for neuroactive compounds to determine if the balance of neuroactive compounds is altered to push the system into an overactive or underactive mode of operation; biochemical and molecular approaches to determine what factors may be altered centrally (spinal cord) or peripherally (dorsal root ganglia, pelvic ganglia, urinary bladder); whole-cell patch clamp recording and intracellular recording from dorsal root ganglion or pelvic ganglion cells to determine if cells are more or less excitable in health or disease; whole animal bladder function testing to evaluate the effects of interventional strategies on bladder function in health and disease; in vitro analysis of urinary bladder strips to assess spontaneous and stimulation evoked changes in contractility.
Zvara P, Braas KM, May V, Vizzard MA. (2006). A role for pituitary adenylate cyclase activating polypeptide (PACAP) in detrusor hyperreflexia after spinal cord injury (SCI). Ann N Y Acad Sci. 1070:622-8. 
Herrera GM, Braas KM, May V, Vizzard MA. (2006). PACAP enhances mouse urinary bladder contractility and is upregulated in micturition reflex pathways after cystitis. Ann N Y Acad Sci. 1070:330-6.
Yuridullah R, Corrow KA, Malley SE, Vizzard MA. (2006). Expression of fractalkine and fractalkine receptor in urinary bladder after cyclophosphamide (CYP)-induced cystitis. Auton Neurosci. 126-127:380-9.
LaBerge J, Malley SE, Zvarova K, Vizzard MA. (2006). Expression of corticotropin-releasing factor and CRF receptors in micturition pathways after cyclophosphamide-induced cystitis. Am J Physiol Regul Integr Comp Physiol. 291(3):R692-703.
Zvarova K, Vizzard MA. (2006). Changes in galanin immunoreactivity in rat micturition reflex pathways after cyclophosphamide-induced cystitis. Cell Tissue Res. 324(2):213-24.
Braas KM, May V, Zvara P, Nausch B, Kliment J, Dunleavy JD, Nelson MT, Vizzard MA. (2006). Role for pituitary adenylate cyclase activating polypeptide in cystitis-induced plasticity of micturition reflexes. Am J Physiol Regul Integr Comp Physiol. 290(4):R951-62.
Vizzard MA. (2006). Neurochemical plasticity and the role of neurotrophic factors in bladder reflex pathways after spinal cord injury. Prog Brain Res. 152:97-115.
Studeny S, Vizzard MA. (2005). Corticotropin-releasing factor (CRF) expression in postnatal and adult rat sacral parasympathetic nucleus (SPN). Cell Tissue Res. 322(3):339-52.
Pictured from left to right: Margaret A. Vizzard, Mary Beth Klinger, Jane Roberts, Lauren Arms, Abbey Dattilio, Kim Corrow, Susan Malley, and Beatrice Girard. Not pictured: Bopaiah Cheppudirah and John Tompkins.
