Veena J, Srikumar B N, Mahati K, Bhagya V, Raju T R, Shankaranarayana Rao B S
Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences, Bangalore, India.
J Neurosci Res. 2009 Mar;87(4):831-43. doi: 10.1002/jnr.21907.
Adult neurogenesis, particularly in the subgranular zone, is thought to be linked with learning and memory. Chronic stress inhibits adult hippocampal neurogenesis and also impairs learning and memory. On the other hand, exposure to enriched environment (EE) is reported to enhance the survival of new neurons and improve cognition. Accordingly, in the present study, we examined whether short-term EE after stress could ameliorate the stress-induced decrease in hippocampal cell proliferation and impairment in radial arm maze learning. After restraint stress (6 hr/day, 21 days) adult rats were exposed to EE (6 hr/day, 10 days). We observed that chronic restraint stress severely affected formation of new cells and learning. Stressed rats showed a significant decrease (70%) in the number of BrdU (5-bromo-2'-deoxyuridine)-immunoreactive cells and impairment in the performance of the partially baited radial arm maze task. Interestingly, EE after stress completely restored the hippocampal cell proliferation. On par with the restoration of hippocampal cytogenesis, short-term EE after stress resulted in a significant increase in percentage correct choices and a decrease in the number of reference memory errors compared with the stressed animals. Also, EE per se significantly increased the cell proliferation compared with controls. Furthermore, stress significantly reduced the hippocampal volume that was reversed after EE. Our observations demonstrate that short-term EE completely ameliorates the stress-induced decrease in cell proliferation and learning deficit, thus demonstrating the efficiency of rehabilitation in reversal of stress-induced deficits and suggesting a probable role of newly formed cells in the effects of EE.
成体神经发生，尤其是在颗粒下区，被认为与学习和记忆有关。慢性应激会抑制成体海马神经发生，同时也会损害学习和记忆。另一方面，据报道，暴露于丰富环境（EE）中可提高新神经元的存活率并改善认知能力。因此，在本研究中，我们研究了应激后短期EE是否能改善应激诱导的海马细胞增殖减少和放射状臂迷宫学习障碍。成年大鼠在经历束缚应激（每天6小时，共21天）后，暴露于EE环境（每天6小时，共10天）。我们观察到慢性束缚应激严重影响新细胞的形成和学习。应激大鼠的BrdU（5-溴-2'-脱氧尿苷）免疫反应性细胞数量显著减少（70%），并且在部分诱饵放射状臂迷宫任务中的表现受损。有趣的是，应激后的EE完全恢复了海马细胞增殖。与海马细胞生成的恢复情况一致，应激后的短期EE与应激动物相比，显著提高了正确选择的百分比，并减少了参考记忆错误的数量。此外，与对照组相比，EE本身显著增加了细胞增殖。此外，应激显著减小了海马体积，而EE后海马体积恢复正常。我们的观察结果表明，短期EE完全改善了应激诱导的细胞增殖减少和学习缺陷，从而证明了康复在逆转应激诱导缺陷方面的有效性，并提示新形成的细胞在EE效应中可能发挥的作用。
