In last years, many experimental and clinical studies helped to create the hypothesis of disturbed glutamatergic transmission in schizophrenia. The hypothesis is based on clinical finding that agonists of NMDA receptors may produce schizophrenia-like symptoms.
Contemporary data confirm that hypofunction of NMDA receptors plays a significant role in pathogenesis of schizophrenia. It seems that the systems: glutamatergic, dopaminergic and serotoninergic are functionally connected in schizophrenia. Classical and atypical neuroleptics may modulate activity of NMDA receptors. The known agonists of NMDA receptors and glycine re-uptake inhibitors seem to be more effective in the treatment of negative than positive schizophrenia symptoms. Their influence on cognitive dysfunctions is also possible. Results of clinical studies suggest that drugs enhancing NMDA receptor activity are more effective in combination with classical or atypical neuroleptic than in monotherapy of schizophrenia.
More clinical trials are necessary to establish the clinical position of drugs producing activation of NMDA receptor.