Development of glutamate binding sites in the visual structures of the rat brain. Effect of visual pattern deprivation.

The postnatal development of the Na-independent 3H-glutamate binding sites has been studied in the retina, lateral geniculate nucleus, superior colliculus, frontal and visual cortex of the rat. In the visual cortex, lateral geniculate nucleus and superior colliculus the highest binding was found at postnatal day 15. Until day 25 glutamate binding decreases drastically reaching the adult values. In contrast, in the retina and in the frontal cortex binding exhibits a maximum already at postnatal day 10 and then decreases to reach the adult value at day 25. Comparing glutamate binding within the visual areas and frontal cortex, highest binding was found in the lateral geniculate nucleus at all stages of age studied. Unilateral eyelid closure from day 11 postnatally resulted in a decreased binding level in the lateral geniculate nucleus ipsilateral to the sutured eye of both 25- and 90-day-old monocularly deprived rats in comparison to controls. A decreased glutamate binding was also observed in the retina of both eyes of 90-day-old monocularly deprived animals, which was not detectable in rats monocularly deprived only until the age of 25 days. The other regions studied were not affected by monocular deprivation. In contrast to that, monocular deprivation until postnatal day 90 failed to affect glutamate high-affinity uptake in both retinas. Binocular deprivation had no effect on glutamate binding in the retina of adult rats. Since monocularly deprived rats use their open eyes for longer periods of time than animals with both eyes open [1], the decreased glutamate binding in the lateral geniculate nucleus might be the consequence of a down-regulation of the increased functional activity of the cortico-geniculate pathway of the non-deprived (open) eye. The decreased glutamate binding in the retina of both eyes of monocularly deprived animals suggests a physiological coupling between both retinas and/or central nervous control of retinal glutamatergic mechanism.