N-Methyl-o-aspartate

Mechanisms of HIV-Induced Neurodegeneration Roles for Excitotoxins and N-Methyl-o-Aspartate Receptors... 

Arendtnielsen L, Petersenfelix S, Fischer M, et al (1995) The effect of N-methyl-o-aspartate antagonist (ketamine) on single and repeated nociceptive stimuli a placebo-controlled experimental human study. Anesth Analg 81 63-68 Areosa SA, Sherriff F (2003) Memantine for dementia (Cochrane Review). Cochrane Database Syst Rev 1 CD003154... 

Unlabeled Uses N-methyl-o-aspartate (NMDA) antagonist in cerebral injury... 

Sur C, Mallorga PJ, Wittmann M, Jacobson MA, Pascarella D, et al. 2003. N-desmethylclozapine, an allosteric agonist at muscarinic 1 receptor, potentiates N-methyl-o-aspartate receptor activity. Proc Natl Acad Sci USA 100 13674-13679. 

Although calcium does not appear to have a direct effect on MGL activity, activation of N-methyl-o-aspartate (NMDA) receptors in spinal cord neurons in... 

Dougherty, P.M., Willis, W.D., 1991. Modification of the responses of primate spinothalamic neurons to mechanical stimulation by excitatory amino acids and an N-methyl-o-aspartate antagonist. Brain Res. 542, 15-22, Suppl. 1. 

Eide, K., Stubhaug, A., Oye, I., Breivik, H., 1995. Continuous subcutaneous administration of the N-methyl-o-aspartic acid (NMDA) receptor antagonist ketamine in the treatment of post-herpetic neuralgia. Pain 61, 221-228. 

Glutamate may serve as a neuroactive substance in nematodes, though no satisfactory demonstrations of cellular localization in subsets of neurons have been made. Membrane-associated binding sites for glutamate have been found in C. elegans and H. contortus (157,158). Glutamate binding is inhibited by aspartate and, to a lesser extent, by quisqualate, but not by kainate or N-methyl-o-aspartate (NMDA). 

Topiramate also antagonizes the effects of glutamate at non-N-methyl-o-aspartate (non-NMDA) receptors, and it also inhibits certain isoenzymes of carbonic anhydrase, although this effect may not be a major feature of its antiepileptic/mood-stabilizing activity. 

This hypothesis is further supported by the similarities between the behavioral effects caused by the administration of N-methyl-o-aspartate (NMDA) receptor antagonists to human subjects and the clinical symptoms of schizophrenia. Moreover, clinical trials in which NMDA receptor activity was enhanced by agents acting at the glycine modulatory site have demonstrated decreases in negative symptoms and variable improvements in cognitive function. There are also data from postmortem studies suggesting alterations in... 

Wolosker, H. Blackshaw, S. Snyder, S.H. Serine racemase a glial enzyme synthesizing o-serine to regulate glutamate-N-methyl-o-aspartate neurotransmission. Proc. Natl. Acad. Sci. USA 1999, 96, 13409-13414. 

Nitroindazole is a selective inhibitor of nNOS, roughly equipotent to other NOS inhibitors (Moore et al. 1993). A comparison of studies shows that 7-nitroindazole given systemically or via the dialysis probe (Babbedge et al. 1993, Moore et al. 1993, Desvignes 1999) shows a similar relationship to that seen with bf -nitro-r-arginine (Salter et al. 1996). 7-Nitroindazole increased extracellular dopamine levels when administered alone and reversed the effects of N-methyl-o-aspartate in the frontal cortex and raphe nuclei of the freely moving rat (Smith and Whitton 2001). 

In specific regions of the optic lobes of Sepia officinalis, stimulation of the N-methyl-o-aspartic acid receptors resulted in a selective decrease in a-tubuhn levels within 30 min with partial recovery after 4 h (Palumbo et al. 2002). The effect was suppressed by the NOS inhibitor N -nitro-L-arginine. Incubation of optic lobes with 3-nitrotyrosine resulted hkewise in a selective loss of a-tubulin, due apparently to incorporation of the amino acid into the C-terminus of detyrosinated a-tubulin to give the nitrated protein purportedly more susceptible to degradation. 

Aquopentacyanoferrate(II), [Fe"H20(CN)5] ", one of the photo degradation products of vasodilator and nitric oxide donor nitroprusside, is a highly potent, competitive, and selective N-methyl-o-aspartate receptor antagonist (Neijt et al. 2001). It blocked N-methyl-D-aspartate-induced depolarisation in rat cortical slices at submicromolar concentrations, whereas responses to a-amino-3-hy-droxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate were not affected. 

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