Region and diagnosis-specific changes in synaptic proteins in schizophrenia and bipolar I disorder

Gray, Laura J., Dean, Brian, Kronsbein, Helena C., Robinson, Phillip J. and Scarr, Elizabeth 2010, Region and diagnosis-specific changes in synaptic proteins in schizophrenia and bipolar I disorder, Psychiatry research, vol. 178, no. 2, pp. 374-380, doi: 10.1016/j.psychres.2008.07.012.

Attached Files
Name Description MIMEType Size Downloads

Title Region and diagnosis-specific changes in synaptic proteins in schizophrenia and bipolar I disorder
Author(s) Gray, Laura J.ORCID iD for Gray, Laura J.
Dean, Brian
Kronsbein, Helena C.
Robinson, Phillip J.
Scarr, Elizabeth
Journal name Psychiatry research
Volume number 178
Issue number 2
Start page 374
End page 380
Total pages 7
Publisher Elsevier
Place of publication Amsterdam, The Netherlands
Publication date 2010-07
ISSN 0165-1781
Notes Aberrant regulation of synaptic function is thought to play a role in the aetiology of psychiatric disorders, including schizophrenia and bipolar disorder. Normal neurotransmitter release is dependent on a complex group of presynaptic proteins that regulate synaptic vesicle docking, membrane fusion and fission, including synaptophysin, syntaxin, synaptosomal-associated protein-25 (SNAP-25), vesicle-associated membrane protein (VAMP), α-synuclein and dynamin I. In addition, structural and signalling proteins such as neural cell adhesion molecule (NCAM) maintain the integrity of the synapse. We have assessed the levels of these important synaptic proteins using Western blots, in three cortical regions (BA10, 40 and 46) obtained post-mortem from subjects with bipolar 1 disorder, schizophrenia or no history of a psychiatric disorder. In bipolar 1 disorder cortex (parietal; BA40), we found a significant increase in the expression of SNAP-25, and a significant reduction in α-synuclein compared with controls. These changes in presynaptic protein expression are proposed to inhibit synaptic function in bipolar 1 disorder. In schizophrenia, a significant reduction in the ratio of the two major membrane-bound forms of NCAM (180 and 140) was observed in BA10. The distinct functions of these two NCAM forms suggest that changes in the comparative levels of these proteins could lead to a destabilisation of synaptic signalling. Our data support the notion that there are complex and region-specific alterations in presynaptic proteins that may lead to alterations in synaptic activity in both schizophrenia and bipolar disorder.
Language eng
DOI 10.1016/j.psychres.2008.07.012
Field of Research 111599 Pharmacology and Pharmaceutical Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2010, Elsevier
Persistent URL

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
Connect to link resolver
Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved.

Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 40 times in TR Web of Science
Scopus Citation Count Cited 43 times in Scopus
Google Scholar Search Google Scholar
Access Statistics: 297 Abstract Views, 0 File Downloads  -  Detailed Statistics
Created: Mon, 17 Aug 2015, 15:36:08 EST

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact