The effects of N-acetylated alpha-linked acidic dipeptidase (NAALADase) inhibitors on [3H]NAAG catabolism in vivo
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Cited by (49)
Maternal inflammation leads to impaired glutamate homeostasis and up-regulation of glutamate carboxypeptidase II in activated microglia in the fetal/newborn rabbit brain
2016, Neurobiology of DiseaseCitation Excerpt :Glutamate-mediated excitotoxicity causes extensive damage to the developing brain in animal models of hypoxia/ischemia (Silverstein et al., 1986). GCPII, previously called N-acetyl-α-linked acidic dipeptidase or NAALADase, catalyzes the hydrolysis of the neuropeptide NAAG to NAA and glutamate (Robinson et al., 1987; Stauch et al., 1989; Serval et al., 1990; Slusher et al., 1992; Fuhrman et al., 1994; Berger et al., 1999). Previous studies have demonstrated that GCPII is expressed in astrocytes in the CNS.
Localization of NAAG-related gene expression deficits to the anterior hippocampus in schizophrenia
2009, Schizophrenia ResearchEffects of NAAG peptidase inhibitor 2-PMPA in model chronic pain - relation to brain concentration
2006, NeuropharmacologyCitation Excerpt :Our in vivo recovery experiment revealed that the concentration of NAAG in the ECF of the rat striatum is approximately 102 nM under physiological conditions. We used no net flux method in the freely moving animal, with a phosphate-containing aCSF since NAAG peptidase is inhibited by phosphate, and in a phosphate-free environment the catabolism of NAAG is increased significantly (Robinson et al., 1987; Stauch et al., 1989; Tortella et al., 2000; Jatzke et al., 2004). We therefore used aCSF with 0.2 mM phosphate, to be as close as possible to physiological conditions (Heipertz et al., 1979).
N-acetylaspartylglutamate and β-NAAG protect against injury induced by NMDA and hypoxia in primary spinal cord cultures
2003, Brain ResearchCitation Excerpt :Specifically, exposure to 8 μM β-NAAG during hypoxia provided 75% protection when viability was assayed the following day, and 63–1000 μM β-NAAG completely eliminated hypoxia-induced loss of viability (107.4–114.4% protection, respectively). To establish the impact of NAAG peptidase activity on the effects of NAAG on cultured spinal cord neurons subjected to excitotoxic insults, we compared responses to NAAG and β-NAAG measured in the phosphate-free media and media containing 1.2 mM sodium phosphate since phosphate is an inhibitor of NAAG peptidase activity [28,32]. As seen in Table 1, neither the NMDA-induced loss of cell viability nor the neuroprotective effects of either NAAG or β-NAAG were affected by the inclusion or exclusion of phosphate in the media.
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Present address: Departments of Pediatrics and Pharmacology, Children's Seashore House, University of Pennsylvania, Philadelphia, PA 19014, U.S.A.
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Present address: Instituto di Ricerche Farmacologiche, ‘Mario Negri’, Via Eritrea 62, 20157 Milan, Italy.