PDF(Pubmed)
Abstract：
The complexity of the classical inverted U-shaped relationship between cortisol levels and responses transposable to stress reactivity has led to an incomplete understanding of the mechanisms enabling healthy and toxic effects of stress on brain and behavior. A clearer, more detailed, picture of those relationships can be obtained by integrating cortisol effects on large-scale brain networks, in particular, by focusing on neural network configurations from the perspective of inhibition and excitation. A unifying view of Semon and Hebb\'s theories of cellular memory links the biophysical and metabolic changes in neuronal ensembles to the strengthening of collective synapses. In that sense, the neuronal capacity to record, store, and retrieve information directly relates to the adaptive capacity of its connectivity and metabolic reserves. Here, we use task-activated cell ensembles or simply engram cells as an example to demonstrate that the adaptive behavioral responses to stress result from collective synapse strength within and across networks of interneurons and excitatory ones.
摘要：
皮质醇水平与可转座为应激反应性的反应之间的经典倒U形关系的复杂性导致对压力对大脑和行为的健康和毒性影响的机制的不完全理解。更清晰的,更详细,这些关系的图片可以通过整合大规模大脑网络上的皮质醇效应来获得，特别是,通过从抑制和激励的角度关注神经网络配置。Semon和Hebb的细胞记忆理论的统一观点将神经元集合中的生物物理和代谢变化与集体突触的加强联系起来。在这个意义上,神经元的记录能力，store,和检索信息直接关系到其连通性和代谢储备的适应能力。这里,我们使用任务激活的细胞集合或简单的Engram细胞作为例子来证明对压力的适应性行为反应是由中间神经元和兴奋性神经元网络内部和之间的集体突触强度引起的。
