(All fields required)
Please enter a valid email.
Please enter your name.
What is : (So we know you are human.)
Please supply the correct answer.
MDB Graduate Student
Understanding the mechanisms of neurological disease onset and progression is an interest of mine, beginning with my undergraduate research in Parkinson’s disease. As a graduate student in the Developmental Biology program at UC under the mentorship of Dr. Danzer my studies now involve adult neurogenesis and aberrant cell integration in the epileptic brain, combining my interests in development and disease.
My research involves studying the structural and functional changes that are observed in models of temporal lobe epilepsy. In particular, I am interested in the involvement of newborn granule cells and the impact of the PTEN/mTOR/AKT pathway on neuronal circuits observed in epilepsy.
Visiting Research Scientist
Treatment of developing animals with commonly used anesthetics has been shown to induce apoptosis. However, the mechanisms underlying this toxicity remain unknown. A genetic fate-mapping approach to label newborn cells in the developing brain has been used as a tool to examine anesthesia-induced neurotoxicity. Using this approach, my research will provide new insights into the long-term impact of anesthetics on developing neuronal populations.
Models of temporal lobe epilepsy have been associated with anatomical and physiological abnormalities in the hippocampal network. My research aims to determine the underlying mechanisms causing structural changes in postnatally generated dentate granule cells in the epileptic brain, as well as determining the role of these abnormal granule cells in creating an epileptic network.
In the rodent model of temporal lobe epilepsy, several distinct morphological changes in the dentate gyrus (DG) neurons of the hippocampus have been identified. It is believed that such changes contribute to the seizure activities associated with epilepsy. My interests are in characterizing and defining how these changes affect the excitability of the individual DG neurons and their connectivity to other neurons in the hippocampus.
Several neurodevelopmental disorders are associated with aberrant neuronal morphology. In particular, disruption of the PI-3 kinase signaling pathway and downstream effectors like mTOR is implicated in autism and epilepsy. By studying gene misexpression in mouse models, primary culture and slice culture, I hope to develop significant insight into changes occurring in these various diseases.
My research interests involve studying the altered morphology present in the hippocampi of the epileptic brain. To this end I use a variety of techniques, including immunohistochemistry, genetic manipulation of target genes and confocal microscopy. My current focus is the Pten knockout model of epilepsy. This model allows us to alter brain structure and function at specific time points during development, leading to epileptiform activity. By examining the structural and functional changes thought to cause seizures, novel treatments could be developed to prevent or reverse these changes.
The integration of abnormal adult born dentate granule cells is implicated in the development of temporal lobe epilepsy. My research interests include studying the effects of altering activity levels in these newborn dentate granule cells as an approach to blocking seizures progression. Further, I am also interested in using different models of epilepsy to study the morphological changes that lead to the development of chronic recurrent seizures.
Steve Danzer, PhDAssociate Professor
Division of Anesthesia3333 Burnet Ave. MLC 2001 Cincinnati, OH 45229
Office Phone: 513-636-4526 Lab Phone: 513-636-6235 Fax: 513-636-7337 Email: email@example.com
3333 Burnet Avenue, Cincinnati, Ohio 45229-3026 | 1-513-636-4200 | 1-800-344-2462 | TTY: 1-513-636-4900
New to Cincinnati Children’s or live outside of the Tristate area? 1-877-881-8479
© 1999-2015 Cincinnati Children's Hospital Medical Center