The role of corticosterone in prehatch-induced memory deficits in chicks.

We have previously shown that prehatch hypoxia (14% oxygen for 24 h), at E10 or E14 of chick embryonic development, produces significant memory deficits, with E10 hypoxia significantly affecting short-term memory and the subsequent formation of long-term memory, whereas E14 hypoxia only affects long-term memory. One of the consequences of hypoxia is the release of stress hormones and we found in this study that hypoxia at E10 or E14 induced a significant increase in circulating corticosterone immediately after the cessation of hypoxia (E11 and E15, respectively). Corticosterone levels remained significantly elevated at hatch in the E14 hypoxia group. This study describes the effect of a single, in ovo, injection of corticosterone on subsequent memory ability in hatched chicks. It was found that corticosterone (0.2 nmol/egg) at E10 or E14 mimicked the memory deficits produced by hypoxia at the same prehatch ages. Embryos treated with corticosterone at E10 had poor short-term memory at hatch, whereas corticosterone administration at E14 resulted in poor long-term memory. Embryos treated with corticosterone at E16 had raised circulating corticosterone levels at hatch, but did not have impaired memory. Treatment with corticosterone at E10, E12, E14 and E16 produced the same cognitive outcomes as hypoxia at the same prehatch ages. However, elevated plasma corticosterone levels at hatch did not necessarily cause the impaired memory processing. Raised levels were observed after treatment at E14 when memory processing was impaired, at E16 when memory was not impaired and not at E10 when memory was impaired. This suggests that an acute rather than sustained increase in plasma corticosterone at particular developmental ages is the cause of impaired memory processing seen at hatch.