The dysfunction of the neurons containing excitatory amino acids is present in a wide range of neurodegenerative disorders. Schizophrenia may also result from a dysfunction of excitatory amino acid neurotransmission. There are two glutamatergic hypotheses of schizophrenia. Glutamate hypofunction hypothesis supposes hypofunction of cerebral glutamatergic neurons in schizophrenia. The most signifi cant consequence of the hypothesis is a possible use of drugs enhancing glutamatergic neurotransmission in the treatment of schizophrenic symptoms. Glutamate hyperfunction hypothesis was also proposed. It suggests a possible effect of glutamate release-inhibiting drugs in schizophrenia.

        Key words: glutamate, schizophrenia, glutamatergic hypothesis, NMDA receptor.