Reduction of Iba1-expressing microglial process density in the hippocampus following electroconvulsive shock.

Recent studies place emphasis on the modulations of immune system in various psychiatric disorders and/or treatments. The aim of this study was to investigate the implications of immune-related glial cells in a rapid-acting treatment for depression, namely, electroconvulsive therapy (ECT). Specifically, the effects of electroconvulsive shock (ECS; animal model of ECT) on microglia were morphologically determined in the mouse hippocampus by using ionized calcium-binding adaptor molecule 1 (Iba1) immunocytochemistry. For comparison, S100beta-positive astrocytes, another type of glial cells, were also tested. After 24 hours of acute ECS administration, a meshwork of Iba1-positive microglial processes was largely diminished, although the change was transient. In mice that received chronic ECS administration, the decline of Iba1-positive microglial process meshwork continued even 1 month after the last shock. Morphometric image analysis revealed the significant reduction of Iba1-positive microglial process density following ECS administration. On the other hand, neither acute nor chronic ECS administration made alterations in the patterns of expression of S100beta immunoreactivity. No significant changes were detected in the cell surface area of S100beta-positive astrocytes following ECS administration. The optical disector analysis demonstrated that ECS did not affect the numerical densities of Iba1-positive microglia and S100beta-positive astrocytes in the hippocampus. These results provide some key to understand the potential role of microglia and astrocytes in the antidepressant action of ECT.