Glycine Site Agonists of the NMDA Receptor: A Review

D’Souza, Deepak Cyril; Charney, Dennis S.; Krystal, John H.

doi:10.1111/j.1527-3458.1995.tb00285.x

Cited by 49 publications

(34 citation statements)

References 159 publications

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“…In recent clinical studies, administration of 30-60 g/day (0.4-0.8 g/kg/day) of glycine was found to induce significant amelioration of negative and cognitive symptoms (reviewed in Heresco-Levy et al 1996). These doses are known to significantly elevate CNS glycine levels (D'Souza et al 1995). Similar results have been obtained with the partial glycine agonist D -cycloserine (Goff et al 1995).…”

supporting

confidence: 73%

Reversal of Phencyclidine-Induced Hyperactivity by Glycine and the Glycine Uptake Inhibitor Glycyldodecylamide

Javitt

Sershen

Hashim

et al. 1997

Neuropsychopharmacology

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supporting

confidence: 73%

Reversal of Phencyclidine-Induced Hyperactivity by Glycine and the Glycine Uptake Inhibitor Glycyldodecylamide

Javitt

Sershen

Hashim

et al. 1997

Neuropsychopharmacology

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“…In addition, investigators have described postmortem evidence of changes in glutamate metabolism and AMPA, kainate, and NMDA receptor expression (Ulas and Cotman., 1997;D'Souza et al, 1995;Akbarian et al, 1996;Gao et al, 2000;Ibrahim et al, 2000;Meador-Woodruff and Healey, 2000;Humphries et al, 1996;Sokolov, 1998) in patients with schizophrenia. These findings and others may be consistent with decreases in optimal NMDA receptor function and/or a disturbance in related circuitry.…”

Section: Evidence For Nmda Receptor Hypofunction In Schizophreniamentioning

confidence: 98%

NMDA receptor regulation of memory and behavior in humans

2001

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N-methyl-D-aspartate (NMDA) receptor hypofunction is associated with a range of effects on cognition and behavior in whole animal and human studies. NMDA receptor hypofunction within the brain, which can be induced experimentally in vivo using NMDA receptor antagonist drugs, produces adverse effects on memory function. The results suggest that NMDA receptor hypofunction can preferentially affect neural mechanisms regulating the efficiency of encoding and consolidation into longer-term storage. More pronounced NMDA receptor hypofunction can produce a clinical syndrome that includes core features of psychosis, as well as dissociation. Finally, sustained and severe underexcitation of NMDA receptors in the adult brain is associated with a neurotoxic process with well-characterized neuropathological features. Progressive increases in severity of NMDA receptor hypofunction within the brain can produce a range of effects on brain function, involving local and distributed circuitry, which may underlie the observed changes in behavior. As the brain ages, the NMDA receptor system becomes progressively hypofunctional, potentially contributing to further age-related decreases in memory and learning performance. Pharmacological and genomic methods for preventing NMDA receptor hypofunction, or for preventing the upstream or downstream consequences modeled by treatment with NMDA antagonists, may be applicable to the prevention and treatment of memory and behavioral dysfunction in a variety of neuropsychiatric disease conditions.

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“…While D-serine and D-cycloserine have high affinity and selectivity for glycine sites of NMDA receptors, glycine is known to have high affinity for inhibitory glycine A receptors, which are distributed primarily in spinal cord and pons (Lynch 2004). Under moderate doses, glycine shows low blood-brain barrier (BBB) permeability (Oldendorph 1971;Toth and Lajtha 1986;D'Souza et al 1995). Furthermore, several studies of both rats and subjects with schizophrenia have suggested that the administration of glycine led to increases in the concentration of D-serine in the central nervous system (CNS) (Takahashi et al 1997;Heresco-Levy et al 2004a).…”

Section: Introductionmentioning

confidence: 99%