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Increased levels of SNAP‐25 and synaptophysin in the dorsolateral prefrontal cortex in bipolar I disorder
Author(s) -
Scarr E,
Gray L,
Keriakous D,
Robinson PJ,
Dean B
Publication year - 2006
Publication title -
bipolar disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.285
H-Index - 129
eISSN - 1399-5618
pISSN - 1398-5647
DOI - 10.1111/j.1399-5618.2006.00300.x
Subject(s) - synaptophysin , snap , dorsolateral prefrontal cortex , syntaxin , prefrontal cortex , neuroscience , bipolar disorder , western blot , synaptic vesicle , schizophrenia (object oriented programming) , hippocampal formation , hippocampus , endocrinology , medicine , biology , psychology , vesicle , exocytosis , immunohistochemistry , psychiatry , biochemistry , gene , cognition , computer graphics (images) , membrane , secretion , computer science
Objective: In order to identify whether the mechanisms associated with neurotransmitter release are involved in the pathologies of bipolar disorder and schizophrenia, levels of presynaptic [synaptosomal‐associated protein‐25 (SNAP‐25), syntaxin, synaptophysin, vesicle‐associated membrane protein, dynamin I] and structural (neuronal cell adhesion molecule and alpha‐synuclein) neuronal markers were measured in Brodmann's area 9 obtained postmortem from eight subjects with bipolar I disorder (BPDI), 20 with schizophrenia and 20 controls. Methods: Determinations of protein levels were carried out using Western blot techniques with specific antibodies. Levels of mRNA were measured using real‐time polymerase chain reaction. Results: In BPDI, levels of SNAP‐25 (p < 0.01) and synaptophysin (p < 0.05) increased. There were no changes in schizophrenia or any other changes in BPDI. Levels of mRNA for SNAP‐25 were decreased in BPDI (p < 0.05). Conclusion: Changes in SNAP‐25 and synaptophysin in BPDI suggest that changes in specific neuronal functions could be linked to the pathology of the disorder.