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Lam et al. (53) study early astrocytic reactivity and microglial activation in the lateral geniculate nucleus (LGN) and visual cortex in ocular hypertensive (OHT) monkeys for up to two months. Sections of the LGN and visual cortex were immunostained with glial fibrillary acidic protein (GFAP) and CD11b (a component of the complement receptor 3b), and markers for astrocytes and microglia, respectively. Background, moderate and robust immunostaining for these markers were described in tissues driven by eye with OHT compared to those driven by the fellow eye.
This study demonstrates astrocytic activation in the visual cortex in early OHT and corroborates previously described glial activation in the LGN in OHT monkeys.1
In this study, microglial activation was not noted in either the LGN or visual cortex (n = 3; Table 1). This is different from an in-vivo study that detected microglia activation by PET with radioactive PK11195 as well as immunostaining for microglia in OHT monkeys.2 Further studies are needed to better understand the temporal course of microglia activation using a larger sample size and multiple markers of microglial activation.3
Unlike the OHT monkeys, the authors found microglial activation in the LGN and primary visual cortex in three animals with optic nerve transection. In view of the active blood-brain barrier disruption and Wallerian degeneration in this model, it is unclear to what extent CD11b is identifying parenchymal microglia or blood-born macrophages in perivascular spaces 4-6 Further studies using CD14 and CD45 will help to clarify this.
Previous work has demonstrated that LGN layers connected to the fellow non-glaucomatous eye undergo degeneration. In this study, since normal controls were not used, it is possible that the use of the fellow eye as a comparator underestimated some of the cellular changes.7 Further studies of inflammatory responses in central visual pathways in glaucoma are needed to investigate whether they are friend or foe at various stages of the disease.