Tsoory M M, Vouimba R M, Akirav I, Kavushansky A, Avital A, Richter-Levin G
Department of Psychology and the Brain and Behavior Research Center, University of Haifa, Haifa, Israel.
Prog Brain Res. 2008;167:35-51. doi: 10.1016/S0079-6123(07)67003-4.
A key assumption in the study of stress-induced cognitive and neurobiological modifications is that alterations in hippocampal functioning after stress are due to an excessive activity exerted by the amygdala on the hippocampus. Research so far focused on stress-induced impairment of hippocampal plasticity and memory but an exposure to stress may simultaneously also result in strong emotional memories. In fact, under normal conditions emotionally charged events are better remembered compared with neutral ones. Results indicate that under these conditions there is an increase in activity within the amygdala that may lead to memory of a different quality. Studying the way emotionality activates the amygdala and the functional impact of this activation we found that the amygdala modulates memory-related processes in other brain areas, such as the hippocampus. However, this modulation is complex, involving both enhancing and suppressing effects, depending on the way the amygdala is activated and the hippocampal subregion examined. The current review summarizes our findings and attempts to put them in context with the impact of an exposure to a traumatic experience, in which there is a mixture of a strong memory of some aspects of the experience but impaired memory of other aspects of that experience. Toward that end, we have recently developed an animal model for the induction of predisposition to stress-related disorders, focusing on the consequences of exposure to stressors during juvenility on the ability to cope with stress in adulthood. Exposing juvenile-stressed rats to an additional stressful challenge in adulthood revealed their impairment to cope with stress and resulted in significant elevation of the amygdala. Interestingly, and similar to our electrophysiological findings, differential effects were observed between the impact of the emotional challenge on CA1 and dentate gyrus subregions of the hippocampus. Taken together, the results indicate that long-term alterations within the amygdala contribute to stress-related mnemonic symptoms and suggest that elucidating further these intra-amygdala alterations and their effects on modulating other brain regions is likely to be beneficial for the development of novel approaches to treat stress-related disorders.
应激诱导的认知和神经生物学改变研究中的一个关键假设是，应激后海马功能的改变是由于杏仁核对海马施加了过度活动。迄今为止，研究主要集中在应激诱导的海马可塑性和记忆损伤，但暴露于应激也可能同时导致强烈的情绪记忆。事实上，在正常情况下，与中性事件相比，充满情感的事件更容易被记住。结果表明，在这些情况下，杏仁核内的活动会增加，这可能导致不同性质的记忆。通过研究情绪如何激活杏仁核以及这种激活的功能影响，我们发现杏仁核会调节其他脑区（如海马）中与记忆相关的过程。然而，这种调节很复杂，取决于杏仁核的激活方式和所检查的海马亚区，既有增强作用也有抑制作用。本综述总结了我们的研究结果，并试图将其与创伤经历暴露的影响联系起来，在创伤经历中，对经历某些方面的记忆很强，但对其他方面的记忆受损。为此，我们最近开发了一种动物模型，用于诱导对应激相关障碍的易感性，重点关注幼年时期暴露于应激源对成年后应对压力能力的影响。成年期将幼年应激大鼠暴露于额外的应激挑战中，发现它们应对压力的能力受损，杏仁核显著升高。有趣的是，与我们的电生理结果类似，在情绪挑战对海马CA1和齿状回亚区的影响之间观察到了差异效应。综上所述，结果表明杏仁核内的长期改变会导致与应激相关的记忆症状，并表明进一步阐明这些杏仁核内的改变及其对调节其他脑区的影响可能有利于开发治疗应激相关障碍的新方法。
