D-cycloserine has been used to inhibit serine hydroxymethyltransferase.[1]
Biochem/physiol Actions
Mode of Action: Inhibits cell wall biosynthesis (D-Ala peptide bond formation). Also prevents conversion of D-Ala to L-Ala. Bacteriostatic. Partial agonist at the glycine modulatory site of NMDA glutamatergic receptors; antibiotic against Gram-negative bacteria. Mode of Resistance: D-Ala transport interference.
Other Notes
Keep container tightly closed in a dry and well-ventilated place.Keep in a dry place.
Administration of benzodiazepines or serotonin reuptake inhibitors in combination with behavior therapy for the treatment of many anxiety disorders has generally lead to only modest gains. In this article we suggest that pharmacotherapy aimed not at treating the symptoms of
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Evolutionary innovations are dependent on mutations. Mutation rates are increased by adverse conditions in the laboratory, but there is no evidence that stressful environments that do not directly impact on DNA leave a mutational imprint on extant genomes. Mutational spectra
Neurobiology of learning and memory, 100, 1-11 (2012-12-04)
It is well established that D-cycloserine (DCS), a partial agonist of the NMDA receptor glycine site, enhances learning and memory processes. Although the effects of DCS have been especially elucidated in the extinction and reconsolidation of aversive behavioral paradigms or
D-cycloserine (DCS) is an N-methyl-D-aspartate (NMDA) receptor partial agonist that facilitates extinction of conditioned fear in animals and cue exposure therapy (CET) for fear and anxiety disorders in people. Recent preclinical and clinical studies have examined the effect of DCS
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