title: Reduction of the small synaptic vesicle protein synaptophysin but not the large dense core chromogranins in the left thalamus of subjects with schizophrenia.
abstract: BACKGROUND
  It has been hypothesized that a lesion in the neuronal circuits of thalamus might contribute to the symptoms in schizophrenia. It has also been suggested that impaired synaptic transmission is an important component of the pathophysiology of schizophrenia. In the present study we assess the synaptic integrity of thalamus by means of examining the protein levels of: (1) synaptophysin, a membrane bound protein of small synaptic vesicles, and (2) chromogranins, a family of soluble secretory proteins stored and released from the secretory large dense-core vesicles.
  
  
  METHODS
  The brains of 9 patients with schizophrenia and 9 age-matched control subjects were studied. The levels of synaptophysin and chromogranins were measured by radioimmunoassays.
  
  
  RESULTS
  The amount of synaptophysin in the left thalamus was significantly decreased (p = .036) in the schizophrenic group (2655 +/- 605 nmol synaptophysin/mg total protein) compared to the control group (3248 +/- 827 nmol synaptophysin/mg total protein). There were no differences between the groups in the levels of chromogranins, nor in the levels of synaptophysin of the right thalamus.
  
  
  CONCLUSIONS
  These findings indicate defect synaptic function in the left thalamus of patients with schizophrenia. This may be the cause of a reduction of synaptic terminals or a defect limited to certain structures of the synapse, namely the small presynaptic vesicles.
authors.affiliation: Department of Psychiatry and Neurochemistry, Göteborg University, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Landén
authors.forename: P
authors.initials: P
authors.lastname: Davidsson
authors.forename: C G
authors.initials: CG
authors.lastname: Gottfries
authors.forename: B
authors.initials: B
authors.lastname: Grenfeldt
authors.forename: M
authors.initials: M
authors.lastname: Stridsberg
authors.forename: K
authors.initials: K
authors.lastname: Blennow
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D001923:Brain Chemistry; D016022:Case-Control Studies; D002864:Chromogranins / Q000032:analysis*; D004292:Dominance, Cerebral; D005260:Female; D006801:Humans; D008297:Male; D012559:Schizophrenia / Q000378:metabolism* / Q000503:physiopathology; D009435:Synaptic Transmission; D016708:Synaptophysin / Q000032:analysis*; D013788:Thalamus / Q000378:metabolism* / Q000473:pathology
chemical_list: D002864:Chromogranins; D016708:Synaptophysin