Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6285391 | Neuroscience Letters | 2010 | 4 Pages |
Abstract
Reduced N-methyl-d-aspartate receptor (NMDAR) function may contribute to the pathogenesis of schizophrenia. Sarcosine, a potent glycine transporter inhibitor, can increase synaptic glycine and then promote NMDAR function. We assessed the antipsychotic potential of sarcosine by comparing the abilities of sarcosine and clozapine to restore the prepulse inhibition (PPI) deficit, hyperlocomotion and regional brain c-Fos expression changes caused by an NMDAR antagonist, ketamine. Four groups of rats were given acute injections, including saline + saline, saline + 30 mg/kg ketamine, 100 mg/kg sarcosine + 30 mg/kg ketamine, and 15 mg/kg clozapine + 30 mg/kg ketamine. Both sarcosine and clozapine reversed the ketamine-induced PPI deficit and hyperlocomotion. They both did not change ketamine-induced increase in c-Fos expression in the prefrontal cortex and nucleus accumbens. However, in the olfactory bulb, sarcosine, but not clozapine, significantly reduced the ketamine-induced increase in c-Fos expression. Our animal study demonstrated that sarcosine may have antipsychotic potential.
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Authors
Shii-Yi Yang, Chen-Jee Hong, Yn-Ho Huang, Shih-Jen Tsai,