Possessing the property of exciting and then poisoning cells or tissues; examples include nerve injury and death produced by glutamate.
[excite + G. toxikon, poison]
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The role of excitotoxic programmed necrosis in acute brain injury.
The endogenous cannabinoid, anandamide, a derivative of arachidonic acid, is synthesized "on demand" from its membrane lipid precursor (28) and as a component of the endocannabinoid system (along with 2-arachidonoyl glycerol) is likely to be involved in maintaining neuronal integrity by protecting neurons from excitotoxic injury (63).
Various physiological mechanisms have been defined for epilepsy The cellular mechanisms of epileptogenesis include cellular damage, gliosis, increased expression of intermediate-early genes (c-fos, c-jun), increased growth factors, neurogenesis, synaptogenesis, alterations of glutamate and GABA signaling, inflammatory mediators, alterations of voltage-gated ion channels, and excitotoxic antibodies [14].
A previous study suggests that these WMH are a consequence of microvascular disease or result from direct neurotoxic effect of Hcy mediated via excitotoxic and apoptotic mechanisms.[5]
In the last few years, melatonin has become the promising option to minimise the neurological sequelae secondary to HIE.16 A study17 demonstrated that melatonin was neuro-protective in a newborn mouse model of excitotoxic white matter lesions mimicking HIE.
Persistent cognitive deficits, induced by intrathecal methotrexate, are associated with elevated CSF concentrations of excitotoxic glutamate analogs and can be reversed by an NMDA antagonist.
Glial expression of interleukin-18 and its receptor after excitotoxic damage in the mouse hippocampus.
The summary of pharmacodynamics is (1) blockade of interneuronal NMDA receptors, (2) disinhibition of pyramidal cells leading to a glutamate surge, (3) activation of the AMPA receptors, (4) blockade of the excitotoxic extrasynaptic NMDA receptors, (5) activation of synaptogenic intracellular signaling and brain-derived neurotropic factor pathways, and (6) stimulation of the mammalian target of rapamycin.
Moreover, as the etiology of nerve cell death in ALS is complex and multifactorial, with excitotoxic mechanisms playing a role together with reduced oxidative metabolism [8], it is relevant to evaluate the effects of a moderate aerobic exercise with controlled intensity determined by CPET and its role on the functional status in ALS patients versus standard care.
The hippocampus shows vulnerability of excitotoxic damage due to rich of glutamatergic synapses [36]; excessive glutamate release and excitotoxicity-induced neurodegeneration in this region may lead to memory and recognition impairment, as seen in patients with DLB.
Indeed, microglia/macrophage cell density was lower in the PB-MNC+ than the PBS group, suggesting that PB-MNC+ may limit the early excitotoxic cascade triggered by ischemia and exert a cerebroprotective effect, as was previously shown following intranasal administration of TGF-[beta] in mice poststroke [34], and therefore have contributed to the significant reduction in infarct volume that we observed.
The pathogenic mechanism is hypothesized excitotoxic injury with delayed neuronal death [2].