Lyn B. Jakeman, Ph.D.

Associate Professor 403 Hamilton Hall 1645 Neil Avenue Columbus  OH  43210-1218 614-688-4424 (office) 614-292-4888 (fax) jakeman.1@osu.edu

Education:
Ph.D., Neuroscience, University of Florida, Gainesville, FL

Lab Focus:
	The failure of axons to successfully regenerate within the injured central nervous system results in permanent sensory, motor, and autonomic loss following spinal cord injury. Research in the Jakeman lab is centered on improving our understanding of the cellular response to injury and thus promoting repair and growth of injured neurons.

Ongoing Research:
Our lab is currently pursuing 3 questions. 1. What distinguishes a permissive from a non-permissive environment? We are currently examining differences in cellular responses to injury across mouse strains using neuroanatomical and behavioral approaches in order to determine the role of non-neuronal cells in the formation of an inhibitory or permissive environment.

2. How can a non-permissive environment be modified to improve the extent of axonal growth after injury? We are currently examining the effects of therapeutic approaches that are directed at altering the proteoglycan composition surrounding the site of injury or enhancing the expression of permissive molecules such as laminins within the lesion site. These in vivo studies are directed at determining the effects of interventions on cellular migration, sprouting, plasticity and functional recovery after injury.

3. We are studying ways to manipulate the permissivity of the lesion environment. The left side of the figure shows the normal astrocyte response to injury, with hypertrophied astrocytes forming a glial scar around the lesion. Axons attempting to grow into the lesion stop at the scar and form endbulbs. The right side of the figure shows a hypothetical manipulated astrocyte response in which astrocytes with an immature phenotype penetrate into the lesion and guide growing axons. One possible source of these cells is the proliferative ependymal zone surrounding the central canal, illustrated on the far left.

Other Collaborations:
Member, The Center for Brain and Spinal Cord Repair
Faculty, Spinal Cord Injury Research Training Program
Adjunct Associate Professor, Department of Neuroscience 

Publications:
	• Ma M, Basso DM, Walters P, Wei P, Stokes BT, Jakeman LB. Behavioral and histological outcomes following graded spinal cord contusion injury in the C57Bl/6 mouse. Exp Neurol 169:239-254, 2001.

• Stokes BT, Jakeman LB. Experimental modelling of human spinal cord injury:  a model that crosses the species barrier and mimics the spectrum of human cytopathology. Spinal Cord 40:101-109, 2002.
• Ma M, Wei T, Boring L, Charo IF, Ransohoff RM, Jakeman LB. Monocyte recruitment and myelin removal are delayed following spinal cord injury in mice with CCR2 chemokine receptor deletion. J Neuroscience Res 68:691-702, 2002.
• Ma M, Wei P, Wei T, Ransohoff RM, Jakeman LB. Enhanced axonal growth at the site of a spinal cord contusion injury in a mouse strain (129X1/SvJ) with a diminished inflammatory response. J Comp Neurol 480:469-486, 2004.
• Ankeny DP, McTigue DM, Jakeman LB. Bone marrow transplants provide tissue protection and directional guidance for axons after contusive spinal cord injury in rats. Exp Neurol 190:17-31, 2004.
• Chen Yi, Chen XY, Jakeman LB, Schalk G, Stokes BT, Wolpaw JR. The impact of a new motor skill on an old one:  H-reflex conditioning affects locomotion in rats. J Neurosci 25(29):6898-906, 2005.
• Basso DM, Fisher LC, Anderson AJ, Jakeman LB, McTigue DM, Popovich PG. The Basso mouse scale for locomotion (BMS) detects differences in recovery after spinal cord injury in five common mouse strains. J Neurotrauma 23(5) 625-659, 2006.
• Jakeman LB, Chen Y, Lucin KM, McTigue DM. Mice lacking L1 cell adhesion molecule have deficits in locomotion and enhanced corticospinal tract sprouting following mild contusion injury to the spinal cord. Eur J Neurosci 23(8):1997-2011, 2006.
• Chen Y, Chen XY, Jakeman LB, Chen L, Stokes BT, Wolpaw JR. 2006. Operant conditioning of H-reflex can correct a locomotor abnormality after spinal cord injury in rats. J Neuroscience 26(48):12537-43.
• Mire E, Tomasset N, Jakeman LB*, Rougon G* 2008. Modulating Sema3A signaling with a L1 mimetic peptide is not sufficient to promote motor recovery and axon regeneration after spinal cord injury.  Molec. Cellular Neuroscience 37(2) 222-235. * Co-senior authors contributed equally. PMID: 17997325.
• Quach TT, Massicotte G, Glasper ER, Belin MF, DeVries AC, Honnorat J, Jakeman LB, Baudry M, Duchemin AM and Kolattukudy PE.  2008 Abnormal dendritic lamination and functional impairments in hippocampus of CRMP3-deficient mice. FASEB J. 22(2):401-409.