Brenda Porter, MD, PhD

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				Brenda Porter, M.D., Ph.D. Assistant Professor of Pediatrics and Neurology Childrens' Hospital of Philadelphia 502C Abramson Research Center (215) 267-426-5210 email: porterb@email.chop.edu Click here for selected publications since Dr. Porter's arrival at Penn RESEARCH INTERESTS I am interested in understanding the cellular and molecular changes that contribute to the development of epilepsy in the immature brain. RESEARCH TECHNIQUES mature animal models of epilepsy ; single neuron RNA expression profiling; immunohistochemistry; seizure electrophysiology both animal and human RESEARCH SUMMARY Epilepsy is one of the most common neurologic conditions, affecting up to 0.5% of all children. My research is focused on three areas. After a prolonged seizure in immature rats there is a dramatic increase in the birth of new dentate granule neurons in the hippocampus. There are also changes in the inhibitory and excitatory neurotransmission of dentate granule neurons that is thought to contribute to the development of spontaneous seizures. After a prolonged seizure mature dentate granule neurons have altered inhibitory and excitatory neurotransmitter receptor expression but immature neurons are unchanged. The current focus is on determining if mature, immature or both populations of dentate granule neurons contribute to dentate hyperexcitability and the development of spontaneous seizures. With the longterm goal of manipulating neurogenesis to influence the development of epilepsy Focal cortical dysplasia is an abnormality of neuronal development, and is the most common cause of surgically treated epilepsy in children. We do not understand how dysplasia causes epilepsy. We have been performing RNA expression profiling of dysplastic neurons, normal appearing neurons adjacent to the dysplasia and more distant "normal' appearing tissue from children with intractable epilepsy to identify molecular markers of dysplasia. A prolonged seizure activates the CREB family of transcription factors and may contribute to the eventual development of epilepsy. We have been studying the role of the CREB family members in the development of spontaneous seizures and the regulation of gene expression. We have been utilizing mice genetically engineered to lack transcription factors CREB or CREM and find differences in their susceptibility to develop epilepsy. KEY WORDS: epilepsy, neural developmental disorders, RNA expression profiles, neurogenesis