Severn B. Churn, Ph.D.
Room 621 Medical Sciences Building
1217 East Marshall Street
P.O. Box 980599 MCV Station
Richmond, VA 23298-0599
B.S., Biology, College of William and Mary, 1984
M.S., Biology, University of Richmond, 1986
Ph.D., Pharmacology, Virginia Commonwealth University, 1991
Postdoctoral Fellowship Department of Neurology
Virginia Commonwealth University, 1994
The primary focus of my laboratory is
characterizing the regulation of neuronal excitability and
synaptic strength. Primarily, I am interested in the signal
transduction systems that modulate neuronal excitability and
receptor function. In addition, we study how these regulatory
mechanisms are altered in head trauma, stroke and epilepsy.
We have focused our efforts on elucidating the calcium-regulated
mechanisms that modulate neuronal excitability and receptor
function in prolonged status epilepticus. Status epilepticus
is a severe, life-threatening seizure condition characterized
by continuous or repeated seizure episodes. Status affects
approximately 150,000 people in the united states/year and
is associated with a significant mortality rate. In addition,
those individuals that survive status go on to develop recurrent
The major projects ongoing in the laboratory focus on three
major areas: 1) Modulation of GABAA receptor function, 2)
Modulation of Ca2+-regulated phosphorylation and dephosphorylation
systems and 3) Regulation of free intracellular Ca2+ homeostasis.
In addition, we have established a sophisticated rodent epilepsy
monitoring facility to precisely measure seizure onset and
test potential antiseizure medications. For more information
on my laboratory, click the research link at the top of the
Churn, S.B. Sombati, S., Jakoi,
E. and DeLorenzo, R.J. 2000.
Knockdown of the alpha subunit of CaM kinase II results in altered neuronal excitability and inhibition of GABAA receptor function. Proceedings of the National Academy of Science, USA. 97(10), 5604-5609.
Kurz, J., Parsons, J.T., Rana,
A, Churn, S.B. 2003.
Translocation and activation of
calcineurin following prolonged status epilepticus in the
rat. Neurobiology of Disease, 14:483-493.
Churn, S.B., Rana, A., Lee, K., Parsons, J.T., DeBlas, A. and DeLorenzo, R.J. 2002.
Calcium/calmodulin-dependent kinase II phosphorylation of the GABAA receptor alpha 1 subunit modulates benzodiazepine binding. Journal of Neurochemistry, 82, 1065-1076.
Kurz, J., Parsons, J.T., Sheets, D., Rana, A. and Churn, S.B. 2001.
A significant increase in both basal and maximal calcineurin activity in the rat pilocarpine model of status epilepticus. Journal of Neurochemistry 78(2):304-315.
Churn, S.B. 1995.
Multifunctional calcium and calmodulin-dependent kinase II in neuronal function and disease. Advances in Neuroimmunology 5:241-259.
Full Citation Listing
:(see also bibliography section)
Society for Neurosciences - http://www.sfn.org/
American Society for Neurochemistry - http://www.asneurochem.org/
American Association for the Advancement of Science - http://sageke.sciencemag.org/
New York Academy of Science - http://www.nyas.org/
American Epilepsy Society - http://www.aesnet.org/
Beta Beta Beta Biological Honor Society
Sigma Xi Honorary Research Society