Role of Neurotrophin 3 in spinal neuroplasticity in rats subjected to cord transection

Abstract

That neuroplasticity occurs in mammalian spinal cord is well known, though the underlying mechanism still awaits elucidation. This study evaluated the role of endogenous Neurotrophin-3 (NT-3) in the spinal neuroplasticity. Following cord transection at the junction between T9 and T10, the hindlimb locomotor functions of rats showed gradual but significant improvement from 7 to 28 days post-operation. Corresponding to this was a significant increase in the level of NT-3 in the cord segments caudal to injury site. Significantly, after NT-3-antibody administration, the spinal transected rats displayed poor hindlimb locomotor functions and a decrease in the number of neurons in spinal laminae VIII-IX. Whether NT-3-antibody was administered, corticospinal tract regeneration and somatosensory evoked potentials could not be detected. Our findings suggested that endogenous NT-3 could play an important role in spinal plasticity in adult spinal cords subjected to transection, possibly through a regulation of neuronal activity in the local circuitry.

Upregulation of eIF-5A1 in the paralyzed muscle after spinal cord transection associates with spontaneous hindlimb locomotor recovery in rats by upregulation of the ErbB, MAPK and neurotrophin signal pathways

“…Spontaneous locomotor functional recovery was observed after spinal cord injury [1,8,9]. In the present study, proteomics analysis revealed differentially expressed protein spots in the gastrocnemius muscle between spinal cord transection (SCT) and normal rats.…”

“…Monkeys and humans subjected to spinal cord hemisection that transects all corticospinal projections on that side typically exhibit a marked ability to recover volitionally guided locomotion [2][3][4][5][6][7]. Partial functional recovery was also observed in spinal cord transected rats [8,9]. The mechanism underlying the above phenomenon could be associated with spontaneous plasticity in the intraspinal circuitry in some animals [10,11].…”

Comparison of the Efficiencies of Three Neural Induction Protocols in Human Adipose Stromal Cells

“…However, NGF and BDNF expression recovered at 1 week and surpassed control levels at 2 weeks following differentiation. Other neuroregulatory factors expressed by ADSCs can also regulate neuronal survival and neurogenesis [36,37], and these changes still need to be clarified. We therefore cannot determine whether dADSCs are better than uADSCs for treating neural injuries, as this comparison requires in vitro and in vivo studies to assess therapeutic effectiveness.…”

The Contralesional Repair Mechanism That Leads to the Recovery of Motor Function After Ischemia in the Primary Motor Cortex

“…Although BDNF may serve an important role in minimizing neuronal apoptosis during ischemia, it has not been linked to promoting neuroplasticity after ischemia (Oliveira et al 2013). However, it has been demonstrated that neurtrophin-3 (NT-3) promotes axonal migration in damaged spinal cords of mice (Yang et al 2009). Evidence of NT-3 promoting neuroplasticity in the spinal cord suggests that NT-3 is likely the neurotrophin responsible for increased neuroplasticity in the brain after ischemia, however, this has yet to be tested (Kamei et al 2007).…”