Dark‐rearing retards the maturation of astrocytes in restricted layers of cat visual cortex

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Abstract
The cat visual cortex develops its mature appearance, i.e., its circuitry and neuronal morphology, during a limited period of postnatal development under the influence of visual experience. The critical period for cortical plasticity, which normally extends from the third to seventh postnatal week, can be prolonged by raising animals in total darkness. The prolongation of the critical period by dark‐rearing is restricted to the cortical layers except layer IV. Besides the influence of afferent activity on the physiology of cortical cells and on the interconnectivity of thalamo‐cortical afferents, visual experience has also been shown to affect the development of glial cells. The present study investigates the effects of dark‐rearing on astroglial characteristics as determined by immunostaining for glial fibrillary acidic protein (GFAP) and the S‐100 protein. The data reveal a retardation of astrocytic maturation in dark‐reared animals, shown by a reduced presence of GFAP immunoreactivity compared to light‐experienced animals. The density of astrocytic cell bodies positive for S‐100 is unaffected by dark‐rearing, suggesting that astroglial proliferation does not rely on afferent activity. However, punctate S‐100 staining in the neuropil, which has been shown to reflect astrocytic processes, was also reduced in certain cortical layers in dark‐reared animals. The effects of dark‐rearing on the expression of GFAP and S‐100 were restricted to the cortical layers except layer IV, i.e., those layers that reveal a prolongation of the critical period for cortical plasticity following dark‐rearing. It is concluded that astrocytic maturation in the visual cortex is influenced by neuronal activity. The coincidence of the location of retarded astrocytic maturation and the prolongation of the critical period for cortical plasticity is discussed in the light of the recent evidence that immature astrocytes may be involved in activity‐dependent plasticity of the visual cortex.