Glutamatergic neurotransmission in schizophrenics

Glutamate is the most abundant amino acid in the brain, where it plays an i mportant role as a well-established major excitatory neurotransmitter in th e central nervous system. it has been suggested that reduced glutamate neur otransmission may be involved in the pathophysiology of schizophrenia. The glutamate hypothesis of schizophrenia postulates alterations in the glutama tergic system as an important neurobiochemical event in the pathophysiology of this group of psychotic disorders. An altered glutamate release from sy naptosomes including a hypofunction of different glutamate receptors (i.e. NMDA receptors) from different brain areas have previously been reported. F urthermore, partial agonists at the glycine co-agonist site of the NMDA rec eptor might be a new approach in the treatment of schizophrenic symptoms bu t further studies are necessary to clarify the role and efficacy of these s ubstances in schizophrenia. Changes in the glutamatergic cortico-striatal c onnections in schizophrenia could precipitate a potential perceptive overst imulation of the neocortex from thalamic input and an inhibiting influence of the striatum on the thalamus would modulate the information input of the cortex, thereby possibly counteracting the disturbed information processin g which is relatively characteristic for schizophrenic psychoses.