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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