Rodricks Candice L, Miller Suzanne L, Jenkin Graham, Gibbs Marie E
Department of Pharmacology, Monash University, Clayton 3800, Victoria, Australia.
Brain Res. 2006 Dec 6;1123(1):34-41. doi: 10.1016/j.brainres.2006.09.028. Epub 2006 Oct 13.
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.
我们之前已经表明，在鸡胚胎发育的第10天或第14天进行孵化前低氧处理（14%氧气，持续24小时）会产生显著的记忆缺陷，第10天的低氧显著影响短期记忆以及随后长期记忆的形成，而第14天的低氧仅影响长期记忆。低氧的后果之一是应激激素的释放，我们在本研究中发现，第10天或第14天的低氧在低氧停止后立即（分别在第11天和第15天）导致循环皮质酮显著增加。在第14天低氧组中，孵化时皮质酮水平仍显著升高。本研究描述了在卵内单次注射皮质酮对孵化后雏鸡后续记忆能力的影响。结果发现，第10天或第14天的皮质酮（0.2 nmol/蛋）模拟了相同孵化前年龄低氧产生的记忆缺陷。在第10天用皮质酮处理的胚胎在孵化时短期记忆较差，而在第14天给予皮质酮则导致长期记忆较差。在第16天用皮质酮处理的胚胎在孵化时循环皮质酮水平升高，但没有记忆受损。在第10天、第12天、第14天和第16天用皮质酮处理产生的认知结果与相同孵化前年龄的低氧相同。然而，孵化时血浆皮质酮水平升高不一定会导致记忆处理受损。在第14天处理后记忆处理受损时、第16天记忆未受损时以及第10天记忆受损时均观察到水平升高。这表明在特定发育年龄血浆皮质酮的急性而非持续增加是孵化时记忆处理受损的原因。
