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Protection by imidazol(ine) drugs and agmatine of glutamate‐induced neurotoxicity in cultured cerebellar granule cells through blockade of NMDA receptor
TLDR
It is concluded that imidazol(ine) drugs and agmatine are neuroprotective against glutamate‐induced necrotic neuronal cell death in vitro and that this effect is mediated through NMDA receptor blockade by interacting with a site located within the NMDA channel pore. Expand
Neuronal Pentraxin 1 Contributes to the Neuronal Damage Evoked by Amyloid-β and Is Overexpressed in Dystrophic Neurites in Alzheimer's Brain
TLDR
Findings show that NP1 is a key factor for the synapse loss, the neurite damage, and the apoptotic neuronal death evoked by Aβ and indicate that Aβ contributes to the pathology of Alzheimer's disease by regulating NP1 expression. Expand
Overexpression of Neuronal Pentraxin 1 Is Involved in Neuronal Death Evoked by Low K+ in Cerebellar Granule Cells*
TLDR
Results indicate that NP1 is part of the gene expression program of apoptotic cell death activated by nondepolarizing culture conditions in cerebellar granule cells. Expand
Glycogen Synthase Kinase 3 Activity Mediates Neuronal Pentraxin 1 Expression and Cell Death Induced by Potassium Deprivation in Cerebellar Granule Cells
TLDR
Results show that both the JNK and GSK3 signaling pathways are the main routes by which potassium deprivation activates apoptotic cell death, and that NP1 overexpression is regulated by G SKS3 activity independently of the PI-3-K/AKT or JNK pathway. Expand
Deciphering the Iron Side of Stroke: Neurodegeneration at the Crossroads Between Iron Dyshomeostasis, Excitotoxicity, and Ferroptosis
TLDR
This review summarizes recent progresses made in understanding the ferroptosis component underlying both ischemic and hemorrhagic stroke subtypes. Expand
Choline Release and Inhibition of Phosphatidylcholine Synthesis Precede Excitotoxic Neuronal Death but Not Neurotoxicity Induced by Serum Deprivation*
TLDR
The results show that the increase in extracellular choline induced by NMDA receptor activation is directly related with excitotoxic cell death and indicate that choline release is an early event of the excitOToxic process produced by inhibition of phosphatidylcholine synthesis and not by activation of membrane phospholipid degradation. Expand
The effect of simvastatin on the proteome of detergent‐resistant membrane domains: Decreases of specific proteins previously related to cytoskeleton regulation, calcium homeostasis and cell fate
TLDR
Comparative proteomics was used to identify which proteins, besides the N‐methyl‐D‐aspartate receptor, change its percentage of association to DRM after treatment of neurons with simvastatin, and these proteins might represent novel targets for neuroprotection. Expand
Iron-loaded transferrin (Tf) is detrimental whereas iron-free Tf confers protection against brain ischemia by modifying blood Tf saturation and subsequent neuronal damage
TLDR
It is established that blood TSAT exerts a critical role in experimental stroke-induced brain damage and the findings suggest that the protective effect of ATf at the neuronal level resides in preventing NMDA-induced HTf uptake and ROS production, which in turn reduces neuronal damage. Expand
NMDA Receptor Overactivation Inhibits Phospholipid Synthesis by Decreasing Choline–Ethanolamine Phosphotransferase Activity
TLDR
Results show that membrane damage by NMDA is preceded by inhibition of phosphate synthesis and not by phospholipid degradation in the early stages of the excitotoxic process, and that NMDA receptor overactivation decreases phosphatidylcholine and phosph atidylethanolamine synthesis by inhibiting choline–ethanolaminophosphotransferase activity. Expand
Overactivation of α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate and N‐methyl‐d‐aspartate but not kainate receptors inhibits phosphatidylcholine synthesis before excitotoxic neuronal death
TLDR
The results show that AMPA, but not kainate, receptor overactivation induces excitotoxic cell death, and that this effect is directly related to the ability to inhibit phosphatidylcholine synthesis. Expand
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