Mary Beth Klinger-Lawrence

Mary Beth Klinger-Lawrence

  • Senior Lecturer

About

Mary Beth Klinger-Lawrence joined the Department of Biology faculty at Norwich University in 2016. She holds a B.S. in biology from Clarkson University and a Ph.D. in neuroscience from the University of Vermont.

Publications

M.B. Klinger, S. Sacks, F. Cervero. “A role for extracellular signal-regulated kinases 1 and 2 (ERK 1/2) in the maintenance of persistent mechanical hyperalgesia in ovariectomized mice.” Neuroscience. 2011 Jan 13; 172:483-493.

M.A. Vizzard, B.M. Girard, M.B. Klinger. “Neurotrophins and visceral pain.” Visceral Pain. Edited by D.E. Bjorling. Kerala, India: Research Signpost: 2009.

M.B. Klinger, M.A. Vizzard. Role of p75NTR in female rat urinary bladder with cyclophosphamide-induced cystitis. Am J Physiol Renal Physiol. 2008 Oct 8; 295(6): F1778-89.

M.B. Klinger, M.A. Vizzard, B.M. Girard. p75NTR expression in rat urinary bladder sensory neurons and spinal cord with cyclophosphamide-induced cystitis. Journal of Comparative Neurology. 2008 Jan 11;507(3): 1379-1392.

M.B. Klinger, A. Dattilio, M.A. Vizzard. Expression of cyclooxygenase-2 (COX-2) in micturition reflex pathways in rats with cyclophosphamide (CYP)-induced cystitis. American Journal of Physiology - Regulatory, Integrative and Comparative Physiology. 2007 Aug; 293(2): R677-85. Epub 2007 May 30.

C.S. Hassler, R.D. Chafin, M.B. Klinger, M.R. Twiss. Application of the biotic ligand model to explain potassium interaction with thallium uptake and toxicity to plankton. Environmental toxicology and chemistry. 2007 Jun; 26(6):1139-45.

Her teaching specialties include neuroscience and neuroanatomy, anatomy & physiology, and cell biology.

Prior to joining us at Norwich, Klinger-Lawrence did postdoctoral research at McGill University, studying the role of the hormone estrogen in spinal cord processing and perception of visceral pain. She also spent four years working as a scientist in the preclinical research industry in Vermont.

Her Ph.D. work examined changes in sensory neuronal pathways due to visceral inflammation.