University of Kentucky
Grade Level at Time of Presentation
Senior
Major
Neuroscience and Psychology
Minor
Sociology
Institution 23-24
University of Kentucky
KY House District #
33
KY Senate District #
6
Faculty Advisor/ Mentor
Meifan Chen, PhD
Department
Spinal Cord and Brain Injury Research Center
Abstract
Spinal cord injury results in loss of motor, sensory, and autonomic functions. Astrocytes, a cell type in the central nervous system, react to injury in a process called astrogliosis that impacts repair. At the site of injury, reactive astrocytes form an astrocytic scar that yields neuroprotective effects. Impaired formation of this scar causes increased tissue damage along with worsened motor recovery. Our lab identified leucine zipper-bearing kinase (LZK) as a key activator of astrogliosis that promotes wound healing after spinal cord injury in mice. This project examines the effect of astrocyte-specific LZK gene manipulation on hind-limb motor recovery following spinal cord injury. To determine the role of LZK on functional recovery post-injury, a complete crush was performed at thoracic level T8. Hindlimb function was measured using i) Basso Mouse Scale, an open field test that assesses gross motor function; and ii) regular horizontal ladder test that measures skilled stepping over 2 months after injury. Analysis demonstrated decreased function following LZK gene deletion. Decreased gross and fine motor function improvement was seen for the LZK-knock out when compared to the control genotype, suggesting that LZK is necessary for functional recovery. This is further suggested through increased gross motor function observed for the LZK-over expression when compared to the control genotype. Further research must be done to determine the role of LZK-over expression in fine motor recovery.
Included in
Astrocytic Contribution to Motor Recovery After Spinal Cord Injury
Spinal cord injury results in loss of motor, sensory, and autonomic functions. Astrocytes, a cell type in the central nervous system, react to injury in a process called astrogliosis that impacts repair. At the site of injury, reactive astrocytes form an astrocytic scar that yields neuroprotective effects. Impaired formation of this scar causes increased tissue damage along with worsened motor recovery. Our lab identified leucine zipper-bearing kinase (LZK) as a key activator of astrogliosis that promotes wound healing after spinal cord injury in mice. This project examines the effect of astrocyte-specific LZK gene manipulation on hind-limb motor recovery following spinal cord injury. To determine the role of LZK on functional recovery post-injury, a complete crush was performed at thoracic level T8. Hindlimb function was measured using i) Basso Mouse Scale, an open field test that assesses gross motor function; and ii) regular horizontal ladder test that measures skilled stepping over 2 months after injury. Analysis demonstrated decreased function following LZK gene deletion. Decreased gross and fine motor function improvement was seen for the LZK-knock out when compared to the control genotype, suggesting that LZK is necessary for functional recovery. This is further suggested through increased gross motor function observed for the LZK-over expression when compared to the control genotype. Further research must be done to determine the role of LZK-over expression in fine motor recovery.