Sex differences in a hypoxia model of preterm brain damage.

Male sex is a well-established risk factor for poor neurodevelopmental outcome after premature birth. The mechanisms behind this sex-related difference are unknown. The damage associated with prematurity can be mimicked in rodents by prolonged exposure to sublethal postnatal hypoxia.

Characterization of a canine model of autosomal recessive retinitis pigmentosa due to a PDE6A mutation.

Purpose: To characterize a canine model of autosomal recessive RP due to a PDE6A gene mutation.

Methods: Affected and breed- and age-matched control puppies were studied by electroretinography (ERG), light and electron microscopy, immunohistochemistry, and assay for retinal PDE6 levels and enzymatic activity.

Results: The mutant puppies failed to develop normal rod-mediated ERG responses and had reduced light-adapted a-wave amplitudes from an early age.

Development of bullwhip neurons in the embryonic chicken retina.

We have recently described large, unipolar neurons (named bullwhip cells) that regulate the proliferation of progenitors in the circumferential marginal zone (CMZ) of the postnatal chicken retina (Fischer et al. [2005] J. Neurosci.

Ultrasound-mediated gene transfer into neuronal cells.

A new field of gene transfer is emerging as a simple, effective means to drive the expression foreign genes in cells: ultrasound-mediated gene transfer or sonoporation. We report here that sonoporation is an effective means of gene transfer for cultured neurons, a cell type that has been difficult to transfect. Neuronal cell types that are effectively sonoporated include chick retinal neurons, chick dorsal forebrain, chick optic tectum, PC12 cells, rat cerebellar neurons and mouse hippocampal neurons.

Glucagon-expressing neurons within the retina regulate the proliferation of neural progenitors in the circumferential marginal zone of the avian eye.

Glucagon-expressing retinal amacrine cells have been implicated in regulating postnatal ocular growth. Furthermore, experimentally accelerated rates of ocular growth increase the number of neurons added to the peripheral edge of the retina. Accordingly, we assayed whether glucagon-expressing neurons within the retina regulate the proliferation of progenitors in the circumferential marginal zone (CMZ) of the postnatal chicken eye.

Transitin, a nestin-related intermediate filament, is expressed by neural progenitors and can be induced in Müller glia in the chicken retina.

The purpose of this study was to test whether transitin, the avian homologue of nestin, is expressed by retinal progenitors in the developing and postnatal chicken. Because nestin has been widely used as a cell-distinguishing marker of neural progenitors in the mammalian nervous system, we expected to find transitin expressed specifically by the neural progenitors of the retina. In early stages of development, transitin is expressed by neural progenitors in the retina and by cells in the developing ciliary body.

Different aspects of gliosis in retinal Muller glia can be induced by CNTF, insulin, and FGF2 in the absence of damage.

Purpose: In response to acute damage, Muller glia in the retina have been shown to dramatically alter their expression of filamentous proteins. Since damaged retinal cells are known to produce growth factors such as insulin-like growth factor (IGF), ciliary neurotrophic factor (CNTF) and fibroblast growth factor (FGF), the altered expression of filaments in Muller glia in response to retinal damage may be induced by some of these factors. The purpose of this study was to assay whether growth factors influence the expression of filamentous proteins in Muller glia in the intact retinas of postnatal chickens.

BMP4 and CNTF are neuroprotective and suppress damage-induced proliferation of Müller glia in the retina.

In response to acute damage, Müller glia in the chicken retina have been shown to be a source of proliferating progenitor-like cells. The secreted factors and signaling pathways that regulate this process remain unknown. The purpose of this study was to test whether secreted factors, which are known to promote glial differentiation during development, regulate the ability of Müller glia to proliferate and become retinal progenitors in response to acute damage in mature retina.

Copper/zinc superoxide dismutase attenuates neuronal cell death by preventing extracellular signal-regulated kinase activation after transient focal cerebral ischemia in mice.

Recent studies have revealed that activation of extracellular signal-regulated kinase (ERK) may contribute to apoptosis, a cell death process involved in oxidative stress. We examined phosphorylation of ERK1/2 and oxidative stress after transient focal cerebral ischemia (FCI) using transgenic (Tg) mice that overexpress copper/zinc superoxide dismutase (SOD1). The mice were subjected to 60 min of middle cerebral artery (MCA) occlusion by intraluminal suture blockade followed by 1, 4, and 24 hr of reperfusion.