منابع مشابه
Requirement for Superoxide in Excitotoxic Cell Death
We tested the pathogenic role of O2-) radicals in excitotoxic injury. Inactivation of the TCA cycle enzyme, aconitase, was used as a marker of intracellular O2- levels, and a porphyrin SOD mimetic was used to scavenge O2-. The selective, reversible, and SOD-sensitive inactivation of aconitase by known O2- generators was used to validate aconitase activity as a marker of O2- generation. Treatmen...
متن کاملPIKfyve regulates CaV1.2 degradation and prevents excitotoxic cell death
Voltage-gated Ca(2+) channels (VGCCs) play a key role in neuronal signaling but can also contribute to cellular dysfunction and death under pathological conditions such as stroke and neurodegenerative diseases. We report that activation of N-methyl-D-aspartic acid receptors causes internalization and degradation of Ca(V)1.2 channels, resulting in decreased Ca(2+) entry and reduced toxicity. Ca(...
متن کاملA role for polyamines in retinal ganglion cell excitotoxic death.
Neuronal death due to excessive activation of N-methyl-d-aspartate (NMDA) receptors is a hallmark of neurodegenerative diseases. The polyamines: putrescine, spermine, and spermidine, bind to specific sites on the NMDA receptor and promote its activation, but their role in NMDA-induced neuronal death is ill defined. In this study, we characterized the role of polyamines in excitotoxic death of r...
متن کاملExtrasynaptic NMDA receptors: mediators of excitotoxic cell death
The N-methyl-D-aspartate (NMDA) type of glutamate receptor is a calcium-permeable ion channel with important functions in the physiology and pathology of the mammalian brain. NMDA receptors are critical for long-lasting, activity-induced changes in synaptic transmission, a process thought to be involved in learning and memory. NMDA receptors also control neuronal survival and cell death. How ca...
متن کاملActivation of calpain I converts excitotoxic neuron death into a caspase-independent cell death.
Glutamate receptor overactivation contributes to neuron death after stroke, trauma, and epileptic seizures. Exposure of cultured rat hippocampal neurons to the selective glutamate receptor agonist N-methyl-d-aspartate (300 microm, 5 min) or to the apoptosis-inducing protein kinase inhibitor staurosporine (300 nm) induced a delayed neuron death. In both cases, neuron death was preceded by the mi...
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ژورنال
عنوان ژورنال: Journal of Experimental Biology
سال: 2005
ISSN: 1477-9145,0022-0949
DOI: 10.1242/jeb.01945