The Pharmacology of Sodium Hydroxyacetate with Observations on the Toxicity of Glycine*†

Riker, Walter F.; Gold, Harry

doi:10.1002/jps.3030311004

Cited by 10 publications

(2 citation statements)

References 10 publications

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“…Both these effects strongly suggest an interference with the normal functioning of the nervous system. Riker & Gold (1942) have noted, in addition, in cats, complete dilatation of the pupil and loss of reaction to light after the administration of glycine.…”

Section: Homentioning

confidence: 90%

Diet and Inborn Errors of Metabolism

Rimington

1950

Br J Nutr

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Section: Homentioning

confidence: 90%

Diet and Inborn Errors of Metabolism

Rimington

1950

Br J Nutr

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“…(122 ) Nevertheless, it was shown that brain glycine levels could be increased in the rat brain following an intra-arterial injection of glycine (123 ) or feeding with a liquid diet containing high levels of glycine. [l24) In humans, administration of glycine was not associated with any significant adverse effects at dosages up to 3 gikg (125) or at 60g per day. (126) Moreover, intragastric administration of glycine antagonised abnormal behaviours induced by phencyclidine in animals)127) This finding, which was supported by more recent studies in which glycine agonists were administered through intracerebroventricular injection,u28-130) promoted clinical trials involving glycinergic therapy for schizophrenia (table III).…”

Section: Glycine Binding Sitementioning

confidence: 99%

The Glutamate Hypothesis of Schizophrenia

Ishimaru

Toru

1997

CNS Drugs

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rating the negative symptoms [7] that are prominent in patients with a chronic course.l 8 ] Antipsychotics render schizophrenia manageable, but do not completely cure the disorder. Explanations other than dopaminergic hyperactivity are required for further understanding of the illness, as well as for therapeutic advancement. As reviewed below, accumulating evidence indicates that the glutamate hypothesis is one such candidate that may provide a more comprehensive view of schizophrenia, into which dopaminergic hyperactivity may be incorporated. .2 Glutamate Levels in Schizophrenic Brains and CSFGlutamate is the major excitatory neurotransmitter in the mammalian brain. [9. 10] Its effects are mediated through binding to a number of receptors: N-methyl-D-aspartate (NMDA), kainate, aamino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) and metabotropic. Glutamate is responsible for not only the classical fast synaptic transmission through non-NMDA receptors, but a long term potentiation through the NMDA receptor. This latter effect underlies neuronal plasticity.lll] Dysfunction in glutamatergic neural transmission is assumed in various neuropsychiatric disor-eNS Drugs 1997 Jan; 7 (1) Recently, Tsai et alP2] performed a postmortem study of brains from patients who had had schizophrenia that focused on N-acetylaspartyl-glutamate (NAAG), a neuropeptide that is highly concentrated in glutamatergic neurons.!22] NAAG is a partial antagonist of NMDA receptors and, more-

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Glycine 56‐40‐6

2004

Sax's Dangerous Properties of Industrial Materials

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The Pharmacology of Sodium Hydroxyacetate with Observations on the Toxicity of Glycine*†

Cited by 10 publications

References 10 publications

Diet and Inborn Errors of Metabolism

Diet and Inborn Errors of Metabolism

The Glutamate Hypothesis of Schizophrenia

Glycine 56‐40‐6

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