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Repeated Electroconvulsive Seizures Increase the Number of Vessel-Associated Macrophages in Rat Hippocampus

Jansson, Linda PhD; Orre, Karin MSc; Tingström, Anders MD, PhD

Journal of ECT:
doi: 10.1097/YCT.0b013e31824d1f82
Original Studies
Abstract

Objectives: We have previously reported that electroconvulsive seizure (ECS)—an animal model of the antidepressant treatment electroconvulsive therapy—causes glial cell activation in hippocampus and other limbic areas. In the current study, we have investigated whether the cellular response to ECS includes recruitment and infiltration of nonresident macrophages into the hippocampal brain parenchyma.

Methods: Adult rats received 1 ECS daily for 10 consecutive days and were then killed at different time points after the last ECS treatment. Brain sections were immunostained for laminin, a matrix protein expressed in the basal membrane of blood vessels, in combination with anti-CD163, which identifies mature blood-borne macrophages. The number of CD163+ cells in the hippocampus was quantified. We also investigated the number of vessel-associated cells expressing CD4 and major histocompatibility complex class II (MHC II). CD4 is mainly expressed by CD4+ T cells, but can also be found on macrophages, monocytes, and activated microglia, whereas MHC II is expressed by macrophages, activated microglia, dendritic cells, and B cells.

Results: Our results demonstrate increased numbers of CD163+ and CD4+ cells following ECS. Most CD4+ cells within the vasculature had a similar morphology to the CD163+ macrophages. No CD163+ cells were detected outside the vessels but a subpopulation of CD4+ cells was seen in the brain parenchyma, here with a morphology resembling microglia. There was a transient increase in the number of blood vessel-associated MHC II+ cells following ECS.

Conclusions: Our observations showed that the cellular response to ECS involves recruitment of blood-derived macrophages, but we could not see any infiltration into the brain parenchyma of these cells.

Author Information

From the Psychiatric Neuromodulation Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.

Received for publication October 31, 2011; accepted January 26, 2012.

Reprints: Anders Tingström, MD, PhD, Psychiatric Neuromodulation Unit, BMC B12, Sölvegatan 17, 221 84 Lund, Sweden (e-mail: anders.tingstrom@med.lu.se).

The authors have no conflicts of interest to report.

Funding for this study was provided by the Swedish Research Council, the Bror Gadelius Foundation, the OM Persson Foundation, and the Swedish Lundbeck Foundation. The study sponsors had no further role in study design, collection, analysis, or interpretation of data or in writing of the report.

© 2012 by Lippincott Williams & Wilkins