Intraocular BDNF promotes ectopic branching, alters motility and stimulates abnormal collaterals in regenerating optic fibers.

A great deal of effort has been invested in using trophic factors and other bioactive molecules to promote cell survival and axonal regeneration in the adult central nervous system. Far less attention has been paid to investigating potential effects that trophic factors may have that might interfere with recovery. In the visual system, BDNF has been previously reported to prevent regeneration.

Abrogation of β-catenin signaling in oligodendrocyte precursor cells reduces glial scarring and promotes axon regeneration after CNS injury.

When the brain or spinal cord is injured, glial cells in the damaged area undergo complex morphological and physiological changes resulting in the formation of the glial scar. This scar contains reactive astrocytes, activated microglia, macrophages and other myeloid cells, meningeal cells, proliferating oligodendrocyte precursor cells (OPCs), and a dense extracellular matrix. Whether the scar is beneficial or detrimental to recovery remains controversial.

Neuronal growth cones respond to laser-induced axonal damage.

Although it is well known that damage to neurons results in release of substances that inhibit axonal growth, release of chemical signals from damaged axons that attract axon growth cones has not been observed. In this study, a 532 nm 12 ns laser was focused to a diffraction-limited spot to produce site-specific damage to single goldfish axons in vitro. The axons underwent a localized decrease in thickness ('thinning') within seconds.

Hematopoietic stem cell transplantation for pediatric patients with primary immunodeficiency diseases at All Children's Hospital/University of South Florida.

We retrospectively analyzed the transplantation outcomes of 31 patients with primary immunodeficiency diseases treated at our center (All Children's Hospital, University of South Florida) since its inception in 1986. The primary immune diseases included severe combined immunodeficiency, Wiscott-Aldrich syndrome, X-linked hyper-IgM syndrome, and chronic granulomatous disease. The age of the patient's at the time of transplant ranged from 1 month to 19 years, and conditioning regimens varied based on the patients underlying disease.

Axonal rearrangement without reexpression of a growth associated marker: evidence from the compression of the retinotectal system in adult goldfish.

Purpose: Growing axons express a number of proteins associated with axonal growth which are thought to be critical for regeneration and sprouting. Whether these proteins are expressed during injury-induced axonal remodeling is tested in this paper.

Methods: The posterior half of the adult goldfish tectum was removed leaving the anterior half intact.

Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury.

Ciliary neurotrophic factor (CNTF) is important for the survival and outgrowth of retinal ganglion cells (RGCs) in vitro. However, in vivo adult RGCs fail to regenerate and subsequently die following axotomy, even though there are high levels of CNTF in the optic nerve. To address this discrepancy, we used immunohistochemistry to analyze the expression of CNTF receptor alpha (CNTFRalpha) in mouse retina and optic nerve following intraorbital nerve crush.

Expression of polysialylated NCAM but not L1 or N-cadherin by regenerating adult mouse optic fibers in vitro.

This study asks if there might be irreversible maturational changes in adult neurons that limit their capacity to regenerate. Retina from adult and embryonic mouse were placed in culture on laminin substrates so that regenerating adult optic fibers could be compared to growing embryonic fibers. Several cell adhesion molecules (CAMs) known to mediate the growth of embryonic neurites on astrocytes were assayed by immunocytochemistry: L1, N-cadherin, and NCAM.

Histopathologic consequences of moderate concussion in an animal model: correlations with duration of unconsciousness.

Although duration of unconsciousness is commonly used as a prognostic index following traumatic brain injury (TBI), few controlled studies have statistically evaluated the relationship between unconsciousness and histologic pathology, particularly after moderate head injury. Using a pendulum-striker concussive device, a reproducible model of TBI in rats was developed. This model is uncomplicated by skull fractures, contusions, or experimenter-induced craniotomies.

Injury induced expression of growth-associated protein-43 in adult mouse retinal ganglion cells in vitro.

In optic fibers, as in most axons of the central nervous system, the axonal growth-associated protein, GAP-43, is abundant during development but absent in adults. Since optic fibers can be induced to regenerate in culture, we examined whether this was associated with an increased expression of GAP-43 in adult mouse optic fibers that were regenerating from organotypic retinal explants on to laminin substrates. We found that simply placing adult mouse retina in culture under serum-free conditions was sufficient to induce GAP-43, which was detectable after about four to five days in vitro, coincident with the initiation of neurite outgrowth.

Rapid initiation of neurite outgrowth onto laminin from explants of adult mouse retina induced by optic nerve crush.

One optic nerve of an adult mouse was crushed in the orbit. After 8 days, both retinas were explanted onto laminin-coated coverslips. Within 24 h, neurites grew out onto this substrate from explants with prior crush and by 48 h two-thirds of explants had neurites.