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  Vol. 58 No. 6, June 2001 TABLE OF CONTENTS
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Reduced Glial Cell Density and Neuronal Size in the Anterior Cingulate Cortex in Major Depressive Disorder

David Cotter, MRCPsych, PhD; Daniel Mackay, BSc; Sabine Landau, PhD; Robert Kerwin, MRCPsych, PhD, DSc; Ian Everall, MRCPsych, PhD

Arch Gen Psychiatry. 2001;58:545-553.

Background  Glial cells are more numerous than neurons in the cortex and are crucial to neuronal function. There is evidence for reduced neuronal size in schizophrenia, with suggestive evidence for reduced glial cell density in mood disorders. In this investigation, we have simultaneously assessed glial cell density and neuronal density and size in the anterior cingulate cortex in schizophrenia, major depressive disorder, and bipolar disorder.

Methods  We examined tissue from area 24b of the supracallosal anterior cingulate cortex in 60 postmortem brain specimens from 4 groups of 15 subjects, as follows: major depressive disorder, schizophrenia, bipolar disorder, and normal controls. Glial cell density and neuronal size and density were examined in all subjects using the nucleator and the optical disector.

Results  Glial cell density (22%) (P = .004) and neuronal size (23%) (P = .01) were reduced in layer 6 in major depressive disorder compared with controls. There was some evidence for reduced glial density in layer 6 (20%) (P = .02) in schizophrenia compared with controls, before adjusting for multiple layerwise comparisons, but there were no significant changes in neuronal size. There was no evidence for differences in glial density or neuronal size in bipolar disorder compared with controls. Neuronal density was similar in all groups to that found in controls.

Conclusion  These findings suggest that there is reduced frontal cortical glial cell density and neuronal size in major depressive disorder.


From the Division of Psychological Medicine and Neuropathology, Sections of Experimental Neuropathology and Psychiatry (Drs Cotter and Everall and Mr Mackay) and Clinical Neuropharmacology (Dr Kerwin), and the Department of Biostatistics and Computing (Dr Landau), Institute of Psychiatry, London, England.

Corresponding author: David R. Cotter, MRCPsych, PhD, Department of Psychological Medicine and Neuropathology, Institute of Psychiatry, DeCrespigny Park, London SE5 8AF, England (e-mail: david.cotter{at}iop.kcl.ac.uk).



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