Results 231 to 240 of about 45,266 (257)
Some of the next articles are maybe not open access.

Excitotoxicity in the Brain

1998
Excitotoxins are a special group of neurotoxic substances that excite somatic and dendritic receptors in such a way that the neurons may die. All excitotoxins are in principle agonists of glutamate receptors in the brain and are structurally related to glutamate.
openaire   +3 more sources

Calcium, ischemia and excitotoxicity

Cell Calcium, 2010
The initial reports regarding a cytotoxic role of calcium ions were published over 30 years ago. In neurons, calcium ions can gain entry into the cell through several mechanisms. These include the over-activation of glutamate receptors (NMDA, AMPA, KA) or of a range of channels and transporters (TRPM2, TRPM7, NCX, ASICs, CaV1.2, and hemichannels ...
Michael Tymianski   +2 more
openaire   +3 more sources

Are aminoglycoside antibiotics excitotoxic?

NeuroReport, 1998
Guinea pigs received gentamicin to induce a profound hearing loss (61 dB auditory threshold shift at 18 kHz). Concomitant administration of maleic or tartaric acid dissolved in dimethyl sulfoxide (DMSO) significantly reduced the threshold shift to < 40 dB. The results have several important implications.
Jochen Schacht, Su Hua Sha
openaire   +3 more sources

The Excitotoxic Concept

1997
This chapter presents an overview of the excitotoxic concept and its putative involvement in hypoxic–ischemic brain damage. Excitotoxicity refers to the central neuronal injury or death induced by glutamate or related excitatory amino acids. Most excitotoxicity is mediated by glutamate receptors, although prolonged exposure to very high concentrations ...
openaire   +2 more sources

Excitotoxic cell death

Journal of Neurobiology, 1992
AbstractExcitotoxicity refers to the ability of glutamate or related excitatory amino acids to mediate the death of central neurons under certain conditions, for example, after intense exposure. Such excitotoxic neuronal death may contribute to the pathogenesis of brain or spinal cord injury associated with several human disease states.
openaire   +3 more sources

The overlooked aspect of excitotoxicity: Glutamate‐independent excitotoxicity in traumatic brain injuries

European Journal of Neuroscience, 2019
AbstractTraumatic brain injury (TBI) is a leading major cause of morbidity and mortality in youth and individuals under 45 year age. A wide variety of cellular and molecular mechanisms have been identified contributing to the pathogenesis of TBI.
Joel Tehse, Changiz Taghibiglou
openaire   +3 more sources

Excitotoxicity in Aging and Dementia

1983
The extracellular concentration of glutamate in the neocortex of human brain may-increase progressively with ageing. Glutamergic nerve terminals seem to be a major source of the amino acid. There is no evidence that the concentration of extracellular glutamate is increased in the neocortex in Alzheimer’s disease.
C. C. T. Smith   +2 more
openaire   +2 more sources

Multiple sclerosis and glutamate excitotoxicity

Reviews in the Neurosciences, 2013
The previous understanding of multiple sclerosis was solely related to neuroinflammation and its harmful effects; however, countless data indicate the importance of some inflammation-independent, neurodegenerative mechanisms associated with mitochondria malfunction, iron deposition and oxidative stress.
Miloš Kostić   +2 more
openaire   +3 more sources

EXCITOTOXICITY AS A STOCHASTIC PROCESS

Clinical and Experimental Pharmacology and Physiology, 1995
SUMMARY1. Neuronal death following excitotoxic insult appears to be a stochastic process involving transition through an intermediate biochemical state.2. Hydrogen ion accumulation in the hours after toxic glutamate exposure may indicate that this transition has occurred.
openaire   +3 more sources

Excitotoxicity in neonatal hypoxia

Mental Retardation and Developmental Disabilities Research Reviews, 2001
AbstractHypoxic‐ischemic encephalopathy (HIE) in neonates is a disorder of excessive neuronal excitation that includes seizures, abnormal EEG activity, and delayed failure of oxidative metabolism with elevated levels of lactic acid in the brain. Evidence from experimental models and clinical investigation indicates that HIE is triggered by a profound ...
openaire   +3 more sources

Home - About - Disclaimer - Privacy