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Journal Article

Citation

Torres-Platas SG, Hercher C, Davoli MA, Maussion G, Labonté B, Turecki G, Mechawar N. Neuropsychopharmacology 2011; 36(13): 2650-2658.

Affiliation

McGill Group for Suicide Studies, Department of Neurology and Neurosurgery, Douglas Mental Health University Institute, McGill University, Verdun, Québec, Canada.

Copyright

(Copyright © 2011, Nature Publishing Group)

DOI

10.1038/npp.2011.154

PMID

21814185

PMCID

PMC3230489

Abstract

Increasing evidence suggests that cortical astrocytic function is disrupted in mood disorders and suicide. The fine neuroanatomy of astrocytes, however, remains to be investigated in these psychiatric conditions. In this study, we performed a detailed morphometric analysis of 3D-reconstructed gray and white matter astrocytes in Golgi-impregnated anterior cingulate cortex (ACC) samples from depressed suicides and matched controls. Postmortem ACC samples (BA24) from 10 well-characterized depressed suicides and 10 matched sudden-death controls were obtained from the Quebec Suicide Brain Bank. Golgi-impregnated protoplasmic astrocytes (gray matter, layer VI) and fibrous astrocytes (adjacent white matter) were reconstructed, and their morphometric features were analyzed using the Neurolucida software. For each cell, the soma size as well as the number, length, and branching of processes were determined. The densities of thorny protrusions found along the processes of both astrocytic subtypes were also determined. Protoplasmic astrocytes showed no significant difference between groups for any of the quantified parameters. However, fibrous astrocytes had significantly larger cell bodies, as well as longer, more ramified processes in depressed suicides, with values for these parameters being about twice as high as those measured in controls. These results provide the first evidence of altered cortical astrocytic morphology in mood disorders. The presence of hypertrophic astrocytes in BA24 white matter is consistent with reports suggesting white matter alterations in depression, and provides further support to the neuroinflammatory theory of depression.Neuropsychopharmacology advance online publication, 3 August 2011; doi:10.1038/npp.2011.154.


Language: en

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