Aims – to discuss the role of glutamatergic transmission abnormality in schizophrenia, with an emphasis on the pathology of the glutamatergic system receptors and on interrelationships between the glutamatergic, dopaminergic and GABA-ergic systems. Moreover, the paper describes the structure and function of glutamic acid receptors, and especially of NMDA receptor, also in the context of experiments with phencyclidine and ketamine.
Review – Numerous research findings suggest an important role of glutamatergic transmission impairment in the pathogenesis of schizophrenia. The action of phencyclidine and ketamine (chemical compounds with a marked affinity to NMDA receptor of the glutamatergic system) results in the onset of symptoms resembling schizophrenia in their clinical pattern. This is regarded as due to an imbalance between the excitiatory action of the glutamatergic system and inhibitory action of the GABA-ergic system, altering function of other neurotransmission systems.
Conclusions – The glutamatergic system dysfunction seems to play and important part in the pathogenesis of schizophrenia. Abnormal function of this system adversely affects the dopaminergic system functioning, which relates to the now commonly accepted dopaminergic hypothesis of schizophrenia. New therapeutic strategies may be developed, since in the field of schizophrenia research various groups became interested in the role of the glutamatergic system.