Excitotoxicity amino acid receptors

Lynch DR, Guttmann RP (2002) Excitotoxicity perspectives based on N-methyl-D-aspartate receptor subtypes. J Pharmacol Exp Ther 300(3) 717-723 Magnuson DS, Knudsen BE, Geiger JD, Brownstone RM, Nath A (1995) Human immunodeficiency virus type 1 tat activates non-N-methyl-D-aspartate excitatory amino acid receptors and causes neurotoxicity. Ann Neurol 37(3) 373-380 Mamdouh Z, Chen X, Kerini LM, Maxfield FR, Muller WA (2003) Targeted recycling of PECAM from endothelial surface-connected compartments during diapedesis. Nature 421(6924) 748-753... 

The somata of neurons respond to axotomy by chromatolysis in the adult 112 those of neonates are more sensitive and degenerate.113 The release of neurotoxins from reactive glia in damaged neuropil (see above) also causes neuronal cell death. Within wounds there are elevated titres of the excitotoxic amino acids, glutamate and aspartate,114 released from damaged neurons and glia,115 which activate A-methyl-D-aspartate (NMDA) receptors on neurons. The resulting raised intracellular levels... 

Excitotoxic amino acid, stimulates the CNS by acting on glutamate receptors. 

Earooqui AA, Horrocks LA (1991) Excitatory amino acid receptors, neural membrane phospholipid metabolism and neurological disorders. Brain Res Rev 16 171-191 Earooqui AA, Horrocks LA (1994) Excitotoxicity and neurological disorders involvement of membrane phospholipids. Int Rev Neurobiol 36 267-323 Earooqui AA, Ong WY, Horrocks LA (2004) Biochemical aspects of neurodegeneration in human brain involvement of neural membrane phospholipids and phospholipases A2. Neurochem Res 29 1961-1977... 

The concept of excitotoxicity was proposed as early as 1957 by Lucas and Newhouse [62] who demonstrated that glutamate is toxic for retinal cells. In the 70s, the work published by Olney and Ho [63] proved that glutamate and similar compounds administered to rodents during the neonatal period lead to acute neurodegeneration in retinal neurones and periventricular structures. Excitotoxicity is related to an excessive flow of calcium into the neurone resulting from an overstimulation due to different categories of excitatory amino acid receptors [64]. An excess of neurotransmitters produces several effects ... 

It is well known that prolonged NMDA glutamate receptor activation results in degeneration of neurons (excitotoxicity). This has been attributed to a large increase in calcium influx, which activates the calmodulin-dependent NOS-1 and leads to sustained elevation of nitric oxide concentrations. The increase in neurodegeneration caused by excitatory amino acids may be due to enhanced oxygen radical formation since superoxide dismutase has a beneficial effect in... 

A conspicuous feature of hypoglycemic brain damage in the rat is neuronal necrosis in the dentate gyrus (Fig. 3.4) of the hippocampus (Auer et al., 1985). This seems to be due to the proximity of the NMDA receptors of the molecular layer of the dentate, to the CSF spaces containing the excitatory amino acid aspartate. A similar picture of dentate necrosis is seen sometimes, in human cases of hypoglycemic coma. Although the concept of excitotoxicity was unknown in 1938, toxicity of some kind was postulated by Arthur Weil, when he noticed dentate gyrus neurons near the CSF were necrotic in rabbits (Weil et al., 1938). 

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