Increased levels of SNAP‐25 and synaptophysin in the dorsolateral prefrontal cortex in bipolar I disorder

E Scarr, L Gray, D Keriakous, PJ Robinson… - Bipolar …, 2006 - Wiley Online Library
E Scarr, L Gray, D Keriakous, PJ Robinson, B Dean
Bipolar disorders, 2006Wiley Online Library
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 …
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.
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