Glutamine, glutamate and GABA in schizophrenia patients and their healthy first-degree relatives: A 1H-MRS study at 7T



Schizophrenia is a devastating, chronic psychiatric disorder that is marked by complex and heterogeneous symptoms. One pharmacological model that has been particularly successful at explaining the positive, negative, and cognitive symptoms associated with schizophrenia is the N-methyl-D-aspartate receptor (NMDAR) hypofunction hypothesis. This model suggests that decreased functioning of glutamatergic NMDA receptors leads to a somewhat paradoxical excess of glutamatergic turnover, resulting in cortical overexcitation. Animal studies have suggested that this increase of cortical glutamatergic transmission is caused by reduced firing of y-aminobutyric acid (GABA)ergic interneurons. However, in subcortical regions, the effects of NMDAR hypofunction are less clear. As the striatum has yet been shown to be involved in psychosis, it is interesting to also assess NMDA hypofunction in the striatum. In the present study, we measured levels of glutamate, glutamine and GABA in vivo using 1-proton magnetic resonance spectroscopy in chronic, medicated schizophrenia patients, healthy first-degree relatives of patients with schizophrenia, and healthy non-relatives. Specifically, we measured GABA, glutamate and glutamine concentrations in the striatum and the visual cortex to examine the NMDA model of schizophrenia both cortically and subcortically.

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