This provides an elegant mechanism for the control of neuronal development: a surplus of neurons is produced, and only those that form the correct connections with the target tissue receive adequate survival factors. (bmj.com)
Oxidative stress1
Ischemic stroke (IS), which constitutes more than 80% of strokes, generally results from reduced blood supply to cerebral tissue resulting in a number of pathological reactions such as oxidative stress, inflammation, and neuronal cell death [ 1 ]. (springer.com)
Glutamate release2
Thus, glutamate release by reversed uptake helps to trigger the ischaemia-evoked current. (nature.com)
Volatile anesthetics at clinically relevant concentrations are neuroprotective in in vivo models of brain ischemia and reduce glutamate release in vivo and in vitro, but they appear to have weaker neuroprotective effects than hypothermia. (silverchair.com)
Cerebral6
The enzyme cytosolic phospholipase A 2 alpha (cPLA 2 α) has been implicated in the progression of cerebral injury following ischemia and reperfusion. (biomedcentral.com)
These results indicate that cPLA 2 α modulates the earliest molecular and injury responses after cerebral ischemia and have implications for the potential clinical use of cPLA 2 α inhibitors. (biomedcentral.com)
We previously demonstrated that cPLA 2 α is a key effector of neurologic injury following cerebral ischemia and reperfusion (I/R) by showing that cPLA 2 α -/- mice have significantly less stroke injury than do wild-type littermate (+/+) mice after transient regional cerebral ischemia [ 5 ]. (biomedcentral.com)
cPLA 2 α-derived arachidonic acid is also tightly coupled to the 5-lipoxygenase enzyme [ 16 ] and in the gerbil model of global cerebral ischemia 15 minutes of reperfusion caused translocation of 5-LO to the neuron membranes and resulted in increased levels of leukotriene C 4 [ 17 ]. (biomedcentral.com)
This dissertation research focused on focal cerebral ischemia, using the middle cerebral artery occlusion model in rats and mice. (ncl.edu.tw)
Previous studies have shown that intracerebral administration of glial cell line-derived neurotrophic factor (GDNF) reduces ischemia-mediated cerebral infarction. (ncl.edu.tw)
Ischemic3
The levels of cPLA 2 α, cyclooxygenase-2, neuronal morphology and reactive oxygen species in the ischemic and contralateral hemispheres were evaluated by light and fluorescent microscopy. (biomedcentral.com)
Neuronal cyclooxygenase-2 induction and PGE 2 concentration were greater in cPLA 2 α +/+ compared to cPLA 2 α -/- ischemic cortex. (biomedcentral.com)
Accumulation of the excitatory neurotransmitter glutamate in ischemic brain tissue contributes to neuronal cell death. (silverchair.com)
Pathological2
Two distinct modes of cell death-necrosis and apoptosis-are involved in pathological neuronal loss, but apoptosis alone is the mechanism of programmed cell death during development. (bmj.com)
The general mechanism of IS is based on reduced blood supply to neuronal tissue, resulting in neuronal cell damage by various pathological reactions. (springer.com)
Slices1
c , Current in 179 control cells, 12 cells in slices exposed to 25 μM NBQX and 200 μM D-AP5 from before ischaemia, or 9 cells in slices preloaded 16 with 1 mM PDC. (nature.com)
Processes1
LncRNA alterations are often associated with a dysregulation of signaling pathways that control multiple neuronal, physiological, and pathophysiological processes. (springer.com)
Brain2
In this review, we discuss the role of lncRNAs in neuronal injury mechanisms and their association with brain neuroprotection. (springer.com)
Accumulation of glutamate in brain tissue during hypoxia or ischemia plays an important role in pathophysiologic events. (silverchair.com)
Cell1
b , Ischaemia-evoked membrane current in single cell. (nature.com)
Damage2
TRPA1 block reduces myelin damage in ischaemia. (nature.com)
Electron microscopy 2 and imaging of dye-filled oligodendrocytes 3 show ischaemia-evoked Ca 2+ -dependent damage to the capacitance-reducing myelin sheaths, which causes loss of action potential propagation. (nature.com)
Suggest1
These data suggest that TRPA1-containing ion channels could be a therapeutic target in white matter ischaemia. (nature.com)