Education | Academic Appointments | Professional Societies | Honorary Societies

Severn B. Churn, Ph.D.

Office Address:

Room 621 Medical Sciences Building
1217 East Marshall Street
P.O. Box 980599 MCV Station
Richmond, VA 23298-0599

Office Phone: (804) 828-0290
Fax: (804) 824-6432
e-mail: schurn@hsc.vcu.edu



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


Research Interests

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 epileptic seizures.
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 page

Selected Publications

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)


Professional Societies

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/


Honorary Societies

Beta Beta Beta Biological Honor Society
Sigma Xi Honorary Research Society