Astrocyte activation in the cat dLGN following monocular retinal inactivation.

Monocular deprivation obstructs the development of visual neural circuits and can impair vision for a lifetime. Effective treatment of this visual disorder, amblyopia, with patching therapy is limited by a short and early critical period, as well as by poor compliance with prescribed treatment. Temporary pharmacological inactivation of the dominant eye has emerged as a means to rapidly correct the effects of monocular deprivation in animal models. Recovery occurs at older ages, and inactivation causes no apparent damage to neural connections within the primary visual pathway. It is unclear what mechanisms protect synaptic connections serving the inactivated eye. Astrocytes are important for the development and maintenance of synapses throughout the nervous system, and can compensate for a prolonged decrease in neural activity. The aim of the current study was to investigate a possible role for astrocytes in mediating the protection of neural connections following monocular inactivation. A significant increase in immunolabeling for glial fibrillary acidic protein (GFAP), a marker for astrocyte activation, was measured within inactivated-eye layers of the dorsal lateral geniculate nucleus from otherwise normal animals. Elevated levels of GFAP persisted even after the period of inactivation wore off, and GFAP was not significantly elevated following monocular deprivation by lid closure. These results implicate astrocyte activation as a possible mechanism that mediates the safeguarding of neural connections during monocular retinal inactivation. The viability of retinal inactivation as a safe and effective treatment for human amblyopia is facilitated by advancing the understanding of its effects within the visual system.