SNAP-25 reduction in the hippocampus of patients with schizophrenia

Peter M. Thompson; Shirley Egbufoama; Marquis P. Vawter

doi:10.1016/S0278-5846(03)00027-7

SNAP-25 reduction in the hippocampus of patients with schizophrenia

Peter M. Thompson, Shirley Egbufoama, Marquis P. Vawter

Psychiatry

Research output: Contribution to journal › Article › peer-review

101 Scopus citations

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.

Original language	English (US)
Pages (from-to)	411-417
Number of pages	7
Journal	Progress in Neuro-Psychopharmacology and Biological Psychiatry
Volume	27
Issue number	3
DOIs	https://doi.org/10.1016/S0278-5846(03)00027-7
State	Published - May 2003

Keywords

Bipolar illness
Exocytosis
NMDA
NR1
SNAP-25
Schizophrenia

ASJC Scopus subject areas

Pharmacology
Biological Psychiatry

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10.1016/S0278-5846(03)00027-7

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title = "SNAP-25 reduction in the hippocampus of patients with schizophrenia",

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.",

keywords = "Bipolar illness, Exocytosis, NMDA, NR1, SNAP-25, Schizophrenia",

author = "Thompson, {Peter M.} and Shirley Egbufoama and Vawter, {Marquis P.}",

note = "Funding Information: We thank William J. Freed, PhD and James Meador-Woodruff, MD, PhD for critical reading of this manuscript. The authors wish to thank Joel E. Kleinman, MD, PhD, Section Chief on Neuropathology, Thomas M. Hyde, MD, PhD and Mary M. Herman, MD and others at the NIMH Clinical Brain Disorders Branch for the generous use of the samples in this study. We also thank John P. Hatch, PhD for statistical analysis help. This work was supported in part by NARSAD Young Investigator Award to PMT and the William Lion Penzner Foundation to MPV. Copyright: Copyright 2017 Elsevier B.V., All rights reserved.",

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N2 - 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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SNAP-25 reduction in the hippocampus of patients with schizophrenia

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Keywords

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