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Minocycline has been demonstrated to be neuroprotective after spinal cord injury (SCI). However, the cellular consequences of minocycline treatment on the secondary injury response are poorly understood. We examined the ability of minocycline to reduce oligodendrocyte apoptosis, microglial/macrophage activation, corticospinal tract (CST) dieback, and lesion(More)
The RIP monoclonal antibody is commonly used to identify oligodendrocytes. Recently, the RIP antigen was identified as 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase), a known non-compact myelin protein [Watanabe, M., Sakurai, Y., Ichinose, T., Aikawa, Y., Kotani, M., Itoh, K., 2006. Monoclonal antibody Rip specifically recognizes 2',3'-cyclic(More)
In the central nervous system, regeneration of injured axons and sprouting of intact axons are suppressed by myelin-derived molecules that bind to the Nogo receptor (NgR). We used a soluble form of the NgR (sNgR), constructed as an IgG of the human NgR extracellular domain, to manipulate plasticity of uninjured primary afferent and descending monoaminergic(More)
A developmental model of spinal cord injury in the embryonic chick was specifically developed to characterize the involvement of caspases in injury-induced oligodendrocyte apoptosis remote from the lesion and the ability of caspase inhibitors to attenuate this process. Developmental apoptosis in the cervical spinal cord increased within the white matter(More)
The exogenous application of recombinant galectin-1 has recently been shown to promote the rate of peripheral nerve regeneration. Endogenous neuronal galectin-1 expression has recently been demonstrated to increase after axotomy. Here we demonstrate a significant increase in the endogenous neuronal expression of galectin-1 mRNA in facial motoneurons after(More)
The neuronal nuclei (NeuN) antibody, which binds to a poorly characterized antigen/antigens, is increasingly being used in several areas of study as a specific marker to identify neuronal populations. Despite the increasing reliance on NeuN as a panneuronal marker, changes of NeuN expression following axonal injury have not yet been examined. In the present(More)
In this report, we examined the possible functions of the cell death protease, caspase-3, in the axotomy-induced apoptosis of facial motoneurons in newborn rodents. Using in situ hybridization and Western blot, we found higher levels of caspase-3 mRNA and pro-caspase-3 protein expression in motoneurons of neonatal and 2-week-old rats than adult rats.(More)
Myelin-derived molecules inhibit axonal regeneration in the CNS. The Long-Evans Shaker rat is a naturally occurring dysmyelinated mutant, which although able to express the components of myelin lacks functional myelin in adulthood. Given that myelin breakdown exposes axons to molecules that are inhibitory to regeneration, we sought to determine whether(More)
Semaphorins are a family of axonal guidance molecules that, by virtue of their chemorepulsive or chemoattractive actions, may be the important factors in determining the success or failure of axonal regeneration in the mature nervous system after injury. Here, we have used two adult mouse models of nervous system injury to evaluate the neuronal expression(More)
Recently, we reported that chronically axotomized rubrospinal neurons survive for up to 1 year in an atrophied state. This finding contrasted previous work suggesting the death of up to 50% of the neurons over time. In the adult mouse, the majority of facial motoneurons appear to be lost as a result of chronic nerve resection. Here, we sought to determine(More)