Rat retinal benzodiazepine receptors are controlled by visual cortical mechanisms

Abstract

[(3)H]flunitrazepam binding was assayed in retinae of 25-day-old rats subjected either to unilateral enucleation at day 15, to intracranial unilateral cutting of the optic nerve at day 17, or to unilateral ablation of the visual cortex at day 17 postnatally. Unilateral enucleation resulted in an enhanced [(3)H]flunitrazepam binding in the retina of the remaining eye by 23% (P < 0.002, two-tailed Student t-test) as compared to unoperated controls. In rats with one optic nerve cut shortly before the optic chiasm, benzodiazepine binding in the retina of the lesioned side was significantly higher by 20.4 +/- 7.6% (P < 0.02, N = 10, paired test) in comparison to that in the retina with the intact optic nerve. Unilateral visual cortex ablation resulted in a 13% decrease (P < 0.02) in [(3)H]flunitrazepam binding in the retina contralateral to the brain lesion. In the lesioned rats of all three groups, the retinal benzodiazepine receptors were no longer capable of being modified by light/dark adaptation as is observed in normal rats. Our data suggest that (i) rat retinal benzodiazepine receptors are under a control from the visual cortex, and (ii) the benzodiazepine receptors of both eyes seem to be mutually tuned, presumably via a cortico-retinal feedback loop and an interhemispheric cortico-cortical information transfer.