title: Asymmetrical changes in the fodrin alpha subunit in the superior temporal cortices in schizophrenia.
abstract: BACKGROUND
  We examined possible abnormalities in neural structural proteins that may underlie morphometric changes reported in the left superior temporal cortices (Brodmann's area 22) of schizophrenics.
  
  
  METHODS
  Particulate proteins of the superior temporal cortices taken at autopsy from 11 schizophrenic and 9 control brains were fractionated by gel electrophoresis. Target proteins, identified by reading their amino acid sequences, were immunoquantified using the specific antibody.
  
  
  RESULTS
  Amino acid sequences of the 150-kDa proteins on sodium dodecyl sulfate/polyacrylamide gel electrophoresis, which were significantly increased on the left side of schizophrenic superior temporal cortices, revealed that they were proteolytic fragments of the alpha subunit of fodrin, a major cytoskeletal protein underlying the plasma membrane. Immunoquantification using the specific antibodies against alpha and beta subunits of fodrin indicated that there exist concomitant decreases in the full-length 240-kDa form and increases in the 150-kDa form of alpha-fodrin with no changes of the 235-kDa form of beta-fodrin in the left superior temporal cortices of the schizophrenic brains.
  
  
  CONCLUSIONS
  The findings may be a possible molecular basis for linking morphometric changes to neurochemical pathophysiology in schizophrenia.
authors.affiliation: Department of Psychiatry, Shinko Hospital, Kobe, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Kitamura
authors.forename: N
authors.initials: N
authors.lastname: Nishino
authors.forename: T
authors.initials: T
authors.lastname: Hashimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Kajimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Shirai
authors.forename: N
authors.initials: N
authors.lastname: Murakami
authors.forename: C Q
authors.initials: CQ
authors.lastname: Yang
authors.forename: X H
authors.initials: XH
authors.lastname: Lin
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: T
authors.initials: T
authors.lastname: Nakai
authors.forename: T
authors.initials: T
authors.lastname: Mita
authors.forename: O
authors.initials: O
authors.lastname: Komure
authors.forename: O
authors.initials: O
authors.lastname: Shirakawa
authors.forename: H
authors.initials: H
authors.lastname: Nakai
mesh_terms: D000368:Aged; D000596:Amino Acids / Q000032:analysis; D015153:Blotting, Western; D001923:Brain Chemistry / Q000502:physiology*; D002352:Carrier Proteins / Q000378:metabolism*; D004591:Electrophoresis, Polyacrylamide Gel; D018728:Entorhinal Cortex / Q000378:metabolism; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D008297:Male; D008840:Microfilament Proteins / Q000378:metabolism*; D008875:Middle Aged; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D017397:Prefrontal Cortex / Q000378:metabolism; D012559:Schizophrenia / Q000378:metabolism*; D013702:Temporal Lobe / Q000378:metabolism*; D013049:Spectrin
chemical_list: D000596:Amino Acids; D002352:Carrier Proteins; D008840:Microfilament Proteins; D009419:Nerve Tissue Proteins; D013049:Spectrin