Microglial cells are sentinel receptors to threat of the nervous system. They form an evenly spaced surveillance-network of resident cells throughout the central nervous system, being more numerous in the white than in the grey matter. While damage to the central nervous system results into activation of microglial cells, even remote activation has been observed in experimental trauma to the peripheral nerve or in experimental autoimmune neuritis.
We have studied microglia activation in rat experimental autoimmune uveitis. The inflammatory lesions in this model affects only the vascular system of the eye. In contrast to the EAN, in which the peripheral nervous system is directly affected, neuronal structures are not primarily involved in uveitis. Microglia activation was studied by immunocytochemistry with monoclonal antibodies ED1, ED2, OX22, OX6 and controls.
With the onset of clinical signs rats microglial
activation within the optic tract could be easily detected by immunostaining
with ED1. Other structures of the optic system such as colliculus superior
and the visual cortex are not affected. The microglial activation is limited
only to the phase of clinical signs. After recovery from clinical disease
microglial activation can no longer be observed.