Free amino acid level determinations in normal and schizophrenic brain

The GABAergic system in schizophrenia

“…In contrast to the study of Perry et al (1979), Cross and colleagues found no difference in GABA levels in the nucleus accumbens and thalamus between the study groups. Ohnuma et al (1999), using a more specific brain region definition than the studies of Korpi et al (1987), Perry et al (1989), or Kutay et al (1989), reported lower GABA levels in BA 9 and 10, but not 11. The PMI was longer in the control group than in the six schizophrenic subjects and possible group sex and medication effects were not ruled out.…”

“…A coherent pattern can be described : lower GAD '( mRNA and protein (Akbarian et al, 1995b ;Guidotti et al, 2000 ;Impagnatiello et al, 1998 ;Volk et al, 2000) is possibly paralleled by lower GABA concentrations (Kutay et al, 1989), less release of GABA (Sherman et al, 1991), lower GAT-1 mRNA (Ohnuma et al, 1999 ;Volk et al, 2001) and up-regulation of GABA A sites (Benes et al, 1992(Benes et al, , 1996bDean et al, 1999 ;Hanada et al, 1987).…”

“…Korpi et al (1987) found no effect of diagnosis on GABA levels in the nucleus accumbens, frontal cortex, and caudate, but GABA was 37n5 % lower in the amygdala in the schizophrenic group compared with controls. Kutay et al (1989) found lower GABA levels in multiple brain regions including the amygdala, the hippocampus, frontal pole, superior temporal cortex and thalamus. Toru et al (1988) (see GAD section above) examined multiple cortical and subcortical regions and noted lower levels only in the posterior portion of the hippocampus of the schizophrenic group.…”

Schizophrenia and viral infection during neurodevelopment: a focus on mechanisms

“…112,113 Synaptosomal release of GABA is likewise thought to be impaired, 112 and GABA itself may be reduced in some brain regions of patients with schizophrenia. 114,115 The decrement of GABA is ostensibly accompanied by a compensatory upregulation of GABA-A receptors. 91 Benes at al have reported a loss of inhibitory interneurons in cingulate and prefrontal cortices, 116 and a decrease in nonpyramidal (presumably inhibitory) neurons in the hippocampus.…”

“…A decrement in glutamatergic function is implied by the finding that glutamate levels are decreased in the hippocampus, prefrontal cortex and CSF, 125,126 but these studies have not been consistently replicated, and there may be increased levels of glutamate in some brain regions. 100,115 Postmortem studies demonstrating a relative decrease of hippocampal complexin II (thought to be a presynaptic marker for excitatory terminals), argue that glutamatergic synapses are impoverished in the disease. 127 This decrement, however, may not be uniformly expressed because the opposite is suggested by increased levels of glutamate reuptake sites in frontal and cingulate cortex, 124,128 and an elevated density of glutamatergic fibers in the anterior cingulate.…”