Memory formation for a weak passive avoidance task in the dark-incubated chicks is facilitated by light exposure or corticosterone administration at optimally pre-hatch time points. To explore the potential mechanisms underlying activation of brain memory function development by light or corticosterone exposure during late embryo, steroid receptor antagonist RU486, or protein synthetic inhibitor anisomycin, was administered intraembryonically to the embryos of either only 24-h light-exposure or complete darkhatched on embryonic day 20 (E20). The results showed that RU486 and anisomycin significantly retarded the facilitated retention both by light and corticosterone exposure in the dark-incubated chicks. They also suggest that the act of corticosterone or light exposure on the development of brain memory function is mediated by the effect of steroid receptor, or afterward on related protein syntheses that is involved in memory formation of post-hatched performance of day-old chicks.
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