Effects of active shock avoidance learning on hippocampal neurogenesis and plasma levels of corticosterone.

摘要

Hippocampal granule neurons that are newly formed during adulthood might be involved in learning and memory processes. Experimental data suggest that only hippocampus-dependent learning tasks stimulate neurogenesis. To further address this issue, the effects of active shock avoidance (ASA) learning on hippocampal progenitor proliferation and survival of newly formed cells were investigated. ASA training, although considered as hippocampus-independent, is known to induce several neurobiological alterations in the hippocampus. Adult Wistar rats were trained in a shuttle box using a 1-day or 4-day paradigm and brains were analyzed for the mitotic marker Ki-67. Effects on survival of newly generated cells were examined by immunocytochemistry for 5-bromo-2-deoxyuridine (BrdU), which was injected 1 week before the training. Neither proliferation nor survival was affected by the ASA learning task. Because elevated glucocorticoid levels have a negative impact on hippocampal neurogenesis, blood samples were taken throughout the 4-day training paradigm. Both trained animals and control rats that were only placed in the shuttle box without receiving foot shocks showed a similar rise in corticosterone, enabling us to exclusively investigate the effects of ASA learning on neurogenesis without differential interference of stress between groups. On the other hand, the finding that ASA induced elevations in plasma corticosterone, but did not influence proliferation or survival of newly formed cells, indicates that this type of stress does not affect neurogenesis. The present study shows that, in line with the existing data on other hippocampus-independent learning tasks, ASA training has no effect on hippocampal neurogenesis.