Abstract
In this study, the authors sought to replicate the findings of reduced synaptosomal associated protein 25 kDa (SNAP-25) immunoreactivity in the hippocampus of patients with schizophrenia. The authors also measured N-methyl-d-aspartate (NMDA) receptor 1 (NR1) receptor subunit to determine if glutamatergic synapses were involved with the loss of SNAP-25. We found 49% less SNAP-25 immunointensity in the schizophrenic group (n=7) compared to the control (n=8) or bipolar groups (n=4) (P=.004). There was no change in NMDA NR1 levels in the three groups. The authors confirm the previous report of less SNAP-25 immunoreactivity in the hippocampus using a different cohort of patients with schizophrenia. It also appears that NMDA NR1 was unchanged, indicating that the overall level of NMDA glutamatergic synapses in hippocampus is normal. These data add to evidence suggesting that in schizophrenia the molecular pathology of the hippocampus involves presynaptic components.
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