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Cingulate cortex synaptic terminal proteins and neural cell adhesion molecule in schizophrenia
1Department of Psychiatry, University of British Columbia, Vancouver, Canada.
Neuroscience
|May 1, 1997
Summary
Schizophrenia alters cingulate cortex synaptic proteins, with elevated syntaxin and neural cell adhesion molecule. This suggests abnormal synaptic function and potentially less mature synapses in this brain region.
Area of Science:
- Neuroscience
- Psychiatry
- Cell Biology
Background:
- Neuronal organization and afferent innervation are altered in the schizophrenia cingulate cortex.
- Synaptic terminal changes are suspected in schizophrenia's cingulate cortex.
Purpose of the Study:
- To investigate synaptic terminal protein alterations in the cingulate cortex in schizophrenia.
- To determine if specific proteins like syntaxin, synaptophysin, and neural cell adhesion molecule are affected.
Main Methods:
- Used immunocytochemistry with monoclonal antibodies (SP6 for syntaxin, SP4 for synaptophysin, SP12 for synaptosomal-associated protein-25).
- Analyzed cingulate cortex tissue from schizophrenia patients and controls.
- Performed multivariate analysis controlling for age and post mortem interval.
Main Results:
- Syntaxin and neural cell adhesion molecule immunoreactivity were significantly elevated in schizophrenia patients compared to controls.
- Syntaxin had a wider distribution than synaptophysin in the cingulate cortex.
- The neural cell adhesion molecule to synaptophysin ratio increased, suggesting less mature synapses.
Conclusions:
- Elevated syntaxin suggests increased glutamatergic afferents in schizophrenia's cingulate cortex.
- Increased neural cell adhesion molecule to synaptophysin ratio indicates potential synaptic immaturity.
- Synaptic function in the cingulate cortex may be abnormal in schizophrenia.