Excitotoxicity is likely to occur in pathological scenarios which mitochondrial function already compromised, shaping neuronal responses glutamate. In fact, mitochondria sustain cell bioenergetics, tune intracellular Ca2+ dynamics, and regulate glutamate availability by using it as metabolic substrate. Here, we suggest the need explore toxicity context of specific disease models may ...

Abstract Excess glutamate in the central nervous system may be a major cause of neurodegenerative diseases with gradual loss and dysfunction neurons. Primary or secondary metabolites from medicinal plants algae show potential for treatment glutamate-induced excitotoxicity. Three plant extracts were evaluated impact on excitotoxicity-induced primary cultures retinal ganglion cells (RGC). These t...

Alzheimer’s disease is the most common form of dementia affecting older adults. also shares a significant association with Major Depressive Disorder. Glutamatergic excitotoxicity via NMDA receptors believed to be key mechanism underlying neurodegeneration in Disease. Blockade by antagonists like Memantine appears inhibit glutamatergic excitotoxicity. increases dopaminergic activation through ag...

Glutamate-mediated excitotoxicity and neurodegeneration have been shown as pathophysiological hallmarks of multiple sclerosis (MS) and other autoimmune inflammatory CNS disorders. N‑Methyl‑D‑Aspartate (NMDA) receptors play a pivotal role in the mediation of neuronal glutamate excitotoxicity leading to cellular damage and apoptotic cell death. Current treatment approaches targeting glutamate exc...

Developing oligodendrocytes (OLs) are highly vulnerable to glutamate excitotoxicity. Although OL excitotoxicity is mainly mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors (AMPARs) and is Ca2+-dependent, the molecular basis for AMPAR-mediated Ca2+ influx in OLs remains largely unclear. Ca2+ permeability of AMPARs is inversely correlated with the abundance of the...

glutamate-mediated excitotoxicity and neurodegeneration have been shown as pathophysiological hallmarks of multiple sclerosis (ms) and other autoimmune inflammatory cns disorders. n‑methyl‑d‑aspartate (nmda) receptors play a pivotal role in the mediation of neuronal glutamate excitotoxicity leading to cellular damage and apoptotic cell death. current treatment approaches targeting glutamate exc...

Excitotoxicity is well recognized as a major pathological process of neuronal death in neurodegenerative diseases involving the central nervous system (CNS). In the animal models of neurodegeneration, excitotoxicity is commonly induced experimentally by chemical convulsants, particularly kainic acid (KA). KA-induced excitotoxicity in rodent models has been shown to result in seizures, behaviora...

Abstract N-methyl-D-aspartate (NMDA) receptor overactivation is involved in neuronal damage after stroke. However, the mechanism underlying NMDA receptor-mediated excitotoxicity remains unclear. In this study, we confirmed that excessive activation of NMDARs led to cell apoptosis in PC12 cells and in primary cultured cortical neurons, which was mediated predominantly by the GluN2B-containing, b...

Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD). However, the mechanism by which excitotoxicity is implicated in neurodegenerative disorders remains unclear. Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in...

metabotropic glutamate receptors (mglurs) consist of a large family of g-protein coupled receptors that are critical for regulating normal neuronal function in the central nervous system. the wide distribution and diverse physiological roles of various mglur subtypes make them highly attractive targets for the treatment of a number of neurological and psychiatric disorders. the discovery of sub...