The glutamatergic compounds sarcosine and N-acetylcysteine ameliorate prepulse inhibition deficits in metabotropic glutamate 5 receptor knockout mice |
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| Authors: | Hwei-Hsien Chen Astrid Stoker Athina Markou |
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| Institution: | (1) Institute of Pharmacology and Toxicology, Tzu Chi University, 701, Section 3, Chung-Yang Road, Hualien, 970, Taiwan;(2) Department of Psychiatry, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0603, USA;(3) Department of Psychopharmacology, Utrecht Institute of Pharmaceutical Science, University of Utrecht, Utrecht, The Netherlands |
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| Abstract: | Rationale Mice lacking metabotropic glutamate receptors 5 (mGluR5) exhibit reduced glutamatergic function and behavioral abnormalities,
including deficits in prepulse inhibition (PPI) of the startle response that may be relevant to schizophrenia. Thus, these
mice are an animal model that may be used for preclinical evaluation of potentially new classes of antipsychotic compounds.
Recent clinical studies have suggested several compounds that modulate glutamatergic transmission through distinct mechanisms,
such as potentiation of the N-methyl-d-aspartate (NMDA) receptor glycine site, activation of group II mGluR, and activation of glutamate-cysteine antiporters, as
being efficacious in the treatment of schizophrenia. |
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