Functional neuroplasticity


Axons in the adult central nervous system (CNS) fail to regenerate after spinal cord injury (SCI), therefore patients with severe SCI remain insensate and paralyzed below the level of the injury. Despite the lack of long distance axon regeneration, partial spontaneous recovery of function is observed in human SCI patients and animal SCI models. Structural plasticity of intact cortical, corticofugal, and spinal circuitry has been suggested to drive this phenomenon. However, the molecular mechanisms underlying functional plasticity of intact circuits remain unknown. 


Research in the Cafferty lab focuses on the capacity of intact CNS circuitry to undergo structural plasticity to drive restoration of function post injury. Using transcriptional profiling, genetics, proteomics, physiology,in vivoneuro-surgical trauma, behavioral studies, biochemistry, tissue culture and chronic two-photon and mesoscale in vivoimaging methodology, we seek to identify and exploit the molecular mechanisms that drive structural plasticity in intact CNS neurons and develop new tools with which to specifically study these pathways to design novel therapies to treat injury and disease of the CNS.