In spinal cord injuries, direct trauma by edges of sublaxated or dislocated vertebrae and indirect ischemia as a result of vascular injury necrotize the neural tissue. After spinal cord injury, tissue loss appears as micro- or macrocavitation. Accumulations of non-neuronal cells substitute spared tissue and halts axon regrowth. Lack of supporting cells (secreting trophic factors and matrix) agg...

The possible role of quercetin, a naturally occurring plant flavonoid, in protecting against oxygen-glucose deprivation (OGD)-, excitotoxins-, and free radical-induced neuronal injury in mouse cortical cell cultures was investigated. Pre- and co-treatment with quercetin (100 microM) inhibited 50 min OGD-, 20 microM N-methyl-D-aspartate (NMDA)-, and 50 microM kainate-induced neurotoxicity by 36,...

Transforming growth factor-β (TGF-β) signaling is involved in pathological processes following brain injury. TGF-β signaling through Smad3 contributes significantly to the immune response and glial scar formation after brain injury. However, TGF-β is also neuroprotective, suggesting that Smad3 signaling may also be involved in neuroprotection after injury. We found expression of the TGF-β type ...

BACKGROUND AND PURPOSE We have previously shown that extracellular acidity protects cultured fetal murine neocortical neurons from glutamate toxicity and combined oxygen-glucose deprivation injury, an action at least in part mediated by reduction in N-methyl-D-aspartate receptor activation. We now investigate the effect of extracellular alkalinity on both glutamate neurotoxicity and injury due ...

Hypoxic-ischemic (HI) brain injury is one of the most severe diseases in the neonatal central nervous system (CNS). The pathological mechanisms of HI brain injury, including cellular apoptosis, excitotoxicity, oxidative stress, etc., are complicated and not well known. Cellular processes such as angiogenesis, neuronal survival and neurogenesis have been proven to be closely associated with brai...

Zhang, Junhui, Geoffrey Thomas Gibney, Peng Zhao, and Ying Xia. Neuroprotective role of -opioid receptors in cortical neurons. Am J Physiol Cell Physiol 282: C1225–C1234, 2002; 10.1152/ajpcell.00226.2001.—We recently demonstrated that -opioid receptor (DOR) activation protects cortical neurons against glutamate-induced injury. Because glutamate is a mediator of hypoxic injury in neurons, we hyp...

Neuronal necrosis and apoptosis occur after traumatic brain injury (TBI) in animals and contribute to subsequent neurological deficits. In contrast, relatively little apoptosis is found after mechanical injury in vitro. Because in vivo trauma models and clinical head injury have associated cerebral ischemia and/or metabolic impairment, we transiently impaired cellular metabolism after mechanica...

Traumatic brain injury (TBI) is a devastating disease that commonly causes persistent mental disturbances and cognitive deficits. Although studies have indicated that overproduction of free radicals, especially superoxide (O2(-)) derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a common underlying mechanism of pathophysiology of TBI, little information is available re...

Little is understood of how damaged white matter interacts with developmental plasticity. The authors propose that computational neuroscience methods are underused in this problem. In this article, they present a nondeterministic, in silico model of activity-dependent plasticity. Using this model, they compared the impact of neuronal cell loss or axonal dysfunction on the ability of the system ...

Purpose: To investigate the effect of FOXO4 on cerebral ischemia/reperfusion (CIR) injury and underlying mechanism.Methods: An in vitro (IR) model was achieved using oxygen-glucose deprivation/reoxygenation (OGD/R). Expression RNA protein determined quantitative real time polymerase chain reaction (qRT-PCR) western blotting, respectively. Cell viability apoptosis were MTT assay flow cytometry, ...