Abstract
The complexity of microglia phenotypes and their related functions compels the continuous study of microglia in diseases animal models. We demonstrated that oxygen-glucose deprivation (OGD) induced rapid, time- and space-dependent phenotypic microglia modifications in CA1 stratum pyramidalis (SP) and stratum radiatum (SR) of rat organotypic hippocampal slices as well as the degeneration of pyramidal neurons, especially in the outer layer of SP. Twenty-four h following OGD, many rod microglia formed trains of elongated cells spanning from the SR throughout the CA1, reaching the SP outer layer where they acquired a round-shaped amoeboid phagocytic head and phagocytosed most of the pyknotic, damaged neurons. NIR-laser treatment, known to preserve neuronal viability after OGD, prevented rod microglia formation. In CA3 SP, pyramidal neurons were less damaged, no rod microglia were found. Thirty-six h after OGD, neuronal damage was more pronounced in SP outer and inner layers of CA1, rod microglia cells were no longer detectable, and most microglia were amoeboid/phagocytic. Damaged neurons, more numerous 36 h after OGD, were phagocytosed by amoeboid microglia in both inner and outer layers of CA1. In response to OGD, microglia can acquire different morphofunctional phenotypes which depend on the time after the insult and on the subregion where microglia are located.
Highlights
Microglia, the resident immune cells of the central nervous system, represent 5–10%of the population of brain cells [1,2]
We assessed whether oxygen glucose deprivation (OGD), an in vitro simil-ischemic insult that causes neurotoxicity [32], evokes activation and/or phenotypic changes of microglia
As apparent in the quantitative analysis of total microglia in the inner and outer stratum pyramidalis (SP) layers and in the Stratum Radiatum (SR) of control, oxygen-glucose deprivation (OGD), OGD+Laser and Laser-treated slices, we demonstrated that there were no significant differences of microglia density in any of these groups (Figure 2)
Summary
The resident immune cells of the central nervous system, represent 5–10%of the population of brain cells [1,2]. Microglia are plastic cells that undergo profound functional modifications in response to damaging stimuli. Factors released by damaged cells polarize microglia toward a M1 phenotype, driving secondary brain injury. Microglia can polarize toward a M2 phenotype, contributing to the suppression of the neuroinflammatory response. Between these extreme functional states, a plethora of possible intermediate states are recognized, among which the Rod microglia phenotype has recently come into focus, raising interest on its still unknown functions [14,15,16,17,18,19]
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