Mitochondrial pathology in human schizophrenic striatum: A postmortem ultrastructural study

Citation
L. King et Rc. Roberts, Mitochondrial pathology in human schizophrenic striatum: A postmortem ultrastructural study, SYNAPSE, 31(1), 1999, pp. 67-75
Citations number
64
Categorie Soggetti
Neurosciences & Behavoir
Journal title
SYNAPSE
ISSN journal
08874476 → ACNP
Volume
31
Issue
1
Year of publication
1999
Pages
67 - 75
Database
ISI
SICI code
0887-4476(199901)31:1<67:MPIHSS>2.0.ZU;2-T
Abstract
Studies using in vivo imaging or microscopic analysis of autopsy specimens indicate abnormalities in the striatum of schizophrenics including lower st riatal metabolism, a change which can be normalized by antipsychotic medica tion. To investigate the possibility that abnormalities in schizophrenia br ain may be due, in part, to pathology in mitochondria, organelles which gen erate energy, postmortem brain tissue from schizophrenic and control cases was obtained from the Maryland Brain Collection. Mitochondria in electron m icrographs of striatal neuropil were counted and digitized. The caudate and the putamen of the schizophrenic subjects contained significantly (P < 0.0 5) fewer (a decrease of approximately 20%) mitochondrial profiles throughou t the neuropil than did normal controls. The numbers of mitochondrial profi les per axon terminal appeared lower in the subset of schizophrenics off-dr ug as compared to either the subset of schizophrenics on-drug or to control s, suggesting that neuroleptic treatment may normalize this measure. The st ructural integrity of mitochondrial profiles in the schizophrenic striata w as not obviously different from that of controls. Fewer mitochondrial profi les suggest decreased energy demands or diminished capacity to respond to e nergy requirements in the structures that contain them. These data are cons istent with other studies showing decreased metabolism in the striatum of s chizophrenics and may identify, in part, the anatomical basis of this defic it. Synapse 31:67-75, 1999. (C) 1999 Wiley-Liss, Inc.