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  • Abstract
    The role of PTPσ in lamprey axon regeneration and cell death after spinal cord injury
    Traumatic spinal cord injury (SCI) results in persistent functional deficits due to the lack of axon regeneration within the mammalian CNS. After SCI, chondroitin sulfate proteoglycans (CSPGs) inhibit axon growth via putative interactions with the LAR-f...
    Oct 20, 2019
  • Abstract
    Control of neuronal excitability by palmitoylation-dependent ion channel clustering at the axon initial segment
    Precise subcellular clustering of neurotransmitter receptors and ion channels is essential for normal synaptic transmission and neuronal excitability. Perhaps the best-studied example of such clustering is at excitatory synapses, where the ‘scaffold’ pr...
    Oct 20, 2019
  • Abstract
    Axon regeneration promoted by signaling of the unfolded protein response in peripheral nerve injury
    The endoplasmic reticulum (ER) has a dynamic interconnected network responsible for maintaining cellular homeostasis including local calcium ion concentration, lipid metabolism and protein synthesis. Multiple cellular malfunctions such as disturbance of...
    Nov 15, 2017
  • Abstract
    Identifying factors that stimulate or improve propriospinal axon regrowth after severe spinal cord injury
    Propriospinal neurons can relay functional information past incomplete spinal cord injuries (SCI) and are good candidates to target for restoring neural connectivity across anatomically complete SCI. Propriospinal neurons do not regrow spontaneously acr...
    Nov 14, 2017
  • Abstract
    The effect of axon resealing time on retrograde neuronal death after spinal cord injury
    Spinal cord injury (SCI) leads to permanent disability in mammals because injured axons do not regenerate across the lesion to reconnect their previous targets. The failure of axon regeneration is due to both extrinsic inhibitory factors, e.g., the chon...
    Nov 13, 2017
  • Abstract
    In vivo analysis of calcium-initiated axon degeneration in an animal model of MS
    Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system and a major cause of neurological disability in young adults. There is robust evidence showing that immune-mediated axon damage is the major cause for progression of...
    Nov 13, 2017
  • Abstract
    Modifying chondroitin sulfation enhances retinal ganglion cell axon regeneration in the mouse optic nerve
    Retinal ganglion cell (RGC) axon regeneration is not spontaneous, but can be induced by inflammation, genetic manipulation, or other stimuli. However, regrowth to central targets is limited in part due to the inhibitory extracellular environment of the ...
    Nov 12, 2017
  • Abstract
    Submicron topographic cues on quasi-2D and 3D substrates to enhance directional axon outgrowth
    Peripheral nerve injury is a debilitating disease characterized by loss of sensation and/or motor function at the affected site. Although fibers in the peripheral nervous system spontaneously regenerates after injury, in many cases, full functional rest...
    Nov 11, 2017
  • Abstract
    Glial proliferation in rat and mouse spinal cord in response to peripheral axon injury
    In previous studies we have shown that transection of the distal cervical sympathetic trunk (CST) results in glial plasticity in the intermediolateral cell column (IML) of the rat and mouse spinal cord, a response that results from the release of retrog...
    Nov 11, 2017
  • Abstract
    Neuronal plasticity and survival in spinal cord following peripheral axon injury: Role of glia
    Previously we reported that transection of distal axons in the cervical sympathetic trunk (CST) leads to robust retrograde neuronal and glial plasticity in the upper thoracic spinal cord. One week following injury the parent sympathetic preganglionic ne...
    Nov 11, 2017
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