Mitochondria in the striatum of subjects with schizophrenia

Abstract

Objectives. Schizophrenia is a severe mental illness that manifests pathology in many brain regions, including the striatum. Among the abnormalities in schizophrenia are those related to mitochondria. The present study sought to determine whether the number of mitochondria was affected at the level of the synapse. Methods. Human postmortem striatum from schizophrenia subjects and controls was examined at the ultrastructural level. The density of mitochondria and synapses were tabulated using stereology. Results. There were similar overall numbers of mitochondria in the caudate nucleus and putamen of schizophrenia subjects vs. controls, but a differential distribution of existing mitochondria. Schizophrenia subjects had 26–30% fewer mitochondria per synapse compared to controls. This may contribute to the pathophysiology of the illness, may be a medication effect, or an adaptive response to normalize the high number of striatal synapses we have previously found. The higher density of mitochondria in dendrites in the caudate nucleus in certain subgroups of schizophrenia vs. controls (>34%) may be related to more synaptic inputs. Conclusions. The role of mitochondria in the various symptoms of schizophrenia is still unclear. A comparison of schizophrenia subjects with differing symptoms or treatment response might shed light on whether differences in mitochondrial density are abnormal or adaptive.

Key words::

• Caudate nucleus
• schizophrenia
• antipsychotics
• neuropathology
• ultrastructure

Acknowledgements

The authors wish to acknowledge the Maryland Brain Collection, especially Drs Carol Tamminga and William T. Carpenter Jr. for diagnosis, and Joy K. Roche for technical support. This research was supported in part by NIH grants MH60744 to RCR and MH073461 to SS.

Statement of interest

Dr. Conley works for Eli Lilly Company.