We are analyzing https://link.springer.com/article/10.1007/s10072-011-0828-5.

Title:
The role of glutamate in neuronal ischemic injury: the role of spark in fire | Neurological Sciences
Description:
Although being a physiologically important excitatory neurotransmitter, glutamate plays a pivotal role in various neurological disorders including ischemic neurological diseases. Its level is increased during cerebral ischemia with excessive neurological stimulation causing the glutamate-induced neuronal toxicity, excitotoxicity, and this is considered the triggering spark in the ischemic neuronal damage. The glutamatergic stimulation will lead to rise in the intracellular sodium and calcium, and the elevated intracellular calcium will lead to mitochondrial dysfunction, activation of proteases, accumulation of reactive oxygen species and release of nitric oxide. Interruption of the cascades of glutamate-induced cell death during ischemia may provide a way to prevent, or at least reduce, the ischemic damage. Various therapeutic options are suggested interrupting the glutamatergic pathways, e.g., inhibiting the glutamate synthesis or release, increasing its clearance, blocking of its receptors or preventing the rise in intracellular calcium. Development of these strategies may provide future treatment options in the management of ischemic stroke.
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Keywords {🔍}

google, scholar, pubmed, article, cas, glutamate, brain, ischemic, cell, ischemia, cerebral, neuronal, calcium, neurosci, receptor, stroke, res, death, nmda, role, excitotoxicity, neurons, sci, biol, pharmacol, focal, neurochem, injury, release, effects, chem, neuroprotective, receptors, neuroprotection, metabotropic, antagonist, ischaemia, cortical, intracellular, mitochondrial, activation, neurotoxicity, acad, effect, rat, treatment, wang, apoptosis, usa, caspase,

Topics {✒️}

n-methyl-d-aspartic acid receptor n-methyl-d-aspartate-mediated neurotoxicity n-methyl-d-aspartic acid-receptors n-methyl-d-aspartate receptor month download article/chapter g-aminobutyric acid studied 3-dihydroxy-6-nitro-7-sulfamoyl-benzo dantrolene-sensitive calcium channels l-type ca2+ channels plasma-stable peptidomimetic inhibitors randomized placebo-controlled trial diaspirin cross-linked hemoglobin kainic acid-induced neurodegeneration calpain-mediated mglur1alpha truncation ampa receptor-mediated excitotoxicity brain-permeable dual blocker cain/cabin1 activates calcineurin long-term secondary prevention l-type calcium channels glutamate-induced neuronal toxicity ligand-operated calcium channels short-term forebrain ischemia synoptically-released zinc contributes mitochondrial nitric-oxide synthase kainate-induced oxidative lesions combined oxygen–glucose deprivation s-100b serum levels glutamate-induced cell death full article pdf calcium-dependent protease calpain metabotropic glutamate receptor nmda receptor subtypes postsynaptic density proteins synthase pdz domain extracellular oxidative/nitrosative stress nmda-induced neurotoxicity ca2+ release channel protein synthesis requirement interleukin-1 receptor antagonist de deyn pp 13 l-type ca privacy choices/manage cookies excitotoxic neuronal death ampa receptor trafficking actin filament depolymerization nmda receptor activities nmda receptor activity oxygen–glucose deprivation metabotropic glutamate receptors neurological disorders

Questions {❓}

Blomgren K, Zhu C, Wang X et al (2001) Synergistic activation of caspase-3 by m-calpain after neonatal hypoxia–ischemia: a mechanism of “pathological apoptosis”?

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