Programa de Pós-graduação em Neurociências, ICBS, Universidade Federal do Rio Grande do Sul, Brazil.
Exp Neurol. 2013 Mar;241:25-33. doi: 10.1016/j.expneurol.2012.11.026. Epub 2012 Dec 6.
Hypoxia-ischemia (HI) is the main cause of mortality in the perinatal period and morbidity, in survivors, which is characterized by neurological disabilities. The immature brain is highly susceptible to hypoxic-ischemic insult and is responsive to environmental stimuli, such as environmental enrichment (EE). Previous results indicate that EE recovered memory deficits in adult rats without reversing hippocampal atrophy related to HI. The aim of this study was to investigate behavioral performance in the open field and rota-rod apparatuses, in object recognition and inhibitory avoidance tasks, as well as dendritic spine density in the hippocampus, in rats undergoing HI and exposed to EE. Seven-day old male rats were submitted to the HI procedure and divided into 4 groups: control maintained in standard environment (CTSE), controls submitted to EE (CTEE), HI in standard environment (HISE) and HI in EE (HIEE). Behavioral and morphological parameters were evaluated 9 weeks after the environmental stimulation. Results indicate impairment in the object recognition task after HI that was recovered by enrichment; however the aversive memory impairment in the inhibitory avoidance task shown by hypoxic-ischemic rats was independent of the environment condition. Hypoxic-ischemic groups showed more crossing responses during the first minute in the open field, when compared to controls, but no differences were found between experimental groups in the rota-rod test. Dendritic spine density in the CA1 subfield of the right hippocampus (ipsilateral to the artery occlusion) was decreased after the HI insult, and increased in enriched controls; interestingly enriched HI rats did not differ from CTSE. In conclusion, EE was effective in recovering declarative memory impairment in object recognition and preserved hippocampal dendritic spine density loss after neonatal HI injury.
缺氧缺血（HI）是围产期死亡和发病率的主要原因，幸存者表现出神经功能障碍。未成熟的大脑对缺氧缺血性损伤高度敏感，并对环境刺激有反应，如环境丰富（EE）。先前的结果表明，EE 恢复了成年大鼠的记忆缺陷，而没有逆转与 HI 相关的海马萎缩。本研究的目的是研究 HI 大鼠在旷场和转棒仪、物体识别和抑制性回避任务中的行为表现，以及海马中的树突棘密度，这些大鼠接受 HI 并暴露于 EE。7 天大的雄性大鼠接受 HI 程序，并分为 4 组：在标准环境中维持的对照组（CTSE）、接受 EE 的对照组（CTEE）、标准环境中的 HI（HISE）和 EE 中的 HI（HIEE）。环境刺激后 9 周评估行为和形态学参数。结果表明，HI 后物体识别任务受损，EE 可恢复；然而，缺氧缺血大鼠在抑制性回避任务中的厌恶记忆损伤与环境条件无关。与对照组相比，缺氧缺血组在旷场试验的第一分钟表现出更多的穿越反应，但实验组在转棒仪试验中没有差异。右侧海马 CA1 亚区（与动脉闭塞相对侧）的树突棘密度在 HI 损伤后减少，而在丰富的对照组中增加；有趣的是，丰富的 HI 大鼠与 CTSE 没有区别。总之，EE 有效恢复了物体识别中的陈述性记忆损伤，并保留了新生 HI 损伤后海马树突棘密度的丧失。
