Although all existing antipsychotic medications have effects on the dopamine system, other neurotransmitter systems are increasingly being recognized as possible therapeutic targets. For instance, the glutamate hypothesis of schizophrenia (Coyle 1996; Goff and Coyle 2001; Javitt and Zukin 1991; Olney and Farber 1995) suggests that modulation of glutamatergic activity could be a potential target for pharmacological treatment of schizophrenia. The glutamate hypothesis is, to a large extent, derived from the observation that treatment of healthy subjects with N-methyl-d-aspartate (NMDA) antagonists, such as ketamine and phencyclidine (PCP), produces symptoms reminiscent of schizophrenia (Adler et al. 1998; Newcomer et al. 1999). Most important, in addition to the psychotic symptoms, which can be induced by a variety of central nervous system stimulants or hallucinogens, NMDA antagonists uniquely produce many of the cognitive deficits associated with schizophrenia (Krystal et al. 1994) and symptoms that resemble the negative symptoms of the illness (Abi-Saab et al. 2001). Thus, it would follow that drugs that enhance NMDA receptor function might be beneficial in the treatment of negative symptoms of schizophrenia (Javitt 2006; Javitt and Coyle 2004).

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