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Douglas A. Coulter, Ph.D.


Associate Professor
Department of Pediatrics, Division of Neurology
Abramson Research Building, Room 410D
34th and Civic Center Boulevard/4318
Phone: (215) 590-1937 FAX: (215) 590-4121
email:   coulterd@email.chop.edu or coulterd@mail.med.upenn.edu
More information on Dr. Coulter

Click here for selected publications since Dr. Coulter's arrival at Penn




RESEARCH INTERESTS

Epilepsy, neuronal excitability, CNS rhythm generation, GABA receptors, development of neurotransmitter receptors and ion channels, synaptic function

RESEARCH TECHNIQUES

Patch clamp recordings, extracellular and intracellular recordings, immunohistochemistry, molecular biology (including aRNA amplification mRNA expression profiling in individual neurons), neuronal cell culture, transgenic animals, in vitro and in vivo recording techniques, optical recordings, EEG recordings.

RESEARCH SUMMARY

My research interests center on understanding the cellular and molecular mechanisms underlying the development of epilepsy. Symptomatic seizure disorders such as temporal lobe epilepsy are among the most prevalent and least medically responsive forms of epilepsy. They are also among the most interesting. A presumably normal individual receives some injurious stimuli, which, at some distant time point results in the initiation of an epileptic state, characterized by recurrent spontaneous seizures. A better understanding these seizure-initiating mechanisms should facilitate development of enhanced therapeutic strategies to improve treatment, and perhaps eventually contribute to the development of a cure for epilepsy.

My laboratory uses physiological, anatomical, and molecular techniques to address experimental issues relevant to epilepsy. Physiologically, my colleagues and I use patch clamp, intracellular, and extracellular recording techniques in both in vitro and in vivo preparations of animal or human brain. Anatomically, we use immunohistochemical and conventional staining techniques to characterize alterations occurring in the epileptic brain at a circuit level, including loss of populations of neurons, alterations in expression patterns of proteins, and axonal remodeling. Molecularly, we use a combination of semi-quantitative profiling of mRNA expression levels at the single cell level, in situ hybridization, retroviral transfection techniques, and antisense oligonucleotide knockdown of expression of certain proteins. The combination of these three diverse experimental approaches provides a powerful, synergistic approach to better understand critical factors contributing to the initiation of the epileptic condition.

KEY WORDS:
epilepsy, hippocampus, GABA receptors, thalamus



 
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