Abstract
The mammalian brain contains high levels of d-serine, which acts as a coagonist at the glycine site of the N-methyl d-aspartate (NMDA)-type glutamate receptor (NMDAR). The synthesis of d-serine from l-serine is catalyzed by serine racemase (SR). To date, several SR knockout (KO) mouse strains have been established to elucidate the role of the SR-d-serine pathway in the regulation of NMDAR activity under both physiological and pathological conditions. Here, we will review the phenotypes of these SR-KO mice used as animal models of NMDAR-mediated neurotoxicity, epilepsy, and schizophrenia and discuss the mechanistic involvement of the SR-d-serine pathway in these neurological and psychiatric disorders.
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