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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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