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反复的应激暴露会导致海马体编码的结构突触不稳定和学习障碍之前。

Repeated stress exposure leads to structural synaptic instability prior to disorganization of hippocampal coding and impairments in learning.

机构信息

Max Planck Institute of Psychiatry, 80804, Munich, Germany.

Graduate School of Systemic Neurosciences GSN-LMU, 82152, Munich, Germany.

出版信息

Transl Psychiatry. 2022 Sep 12;12(1):381. doi: 10.1038/s41398-022-02107-5.

Abstract

Stress exposure impairs brain structure and function, resulting in cognitive deficits and increased risk for psychiatric disorders such as depression, schizophrenia, anxiety and post-traumatic stress disorder. In particular, stress exposure affects function and structure of hippocampal CA1 leading to impairments in episodic memory. Here, we applied longitudinal deep-brain optical imaging to investigate the link between changes in activity patterns and structural plasticity of dorsal CA1 pyramidal neurons and hippocampal-dependent learning and memory in mice exposed to stress. We found that several days of repeated stress led to a substantial increase in neuronal activity followed by disruption of the temporal structure of this activity and spatial coding. We then tracked dynamics of structural excitatory connectivity as a potential underlying cause of the changes in activity induced by repeated stress. We thus discovered that exposure to repeated stress leads to an immediate decrease in spinogenesis followed by decrease in spine stability. By comparison, acute stress led to stabilization of the spines born in temporal proximity to the stressful event. Importantly, the temporal relationship between changes in activity levels, structural connectivity and activity patterns, suggests that loss of structural connectivity mediates the transition between increased activity and impairment of temporal organization and spatial information content in dorsal CA1 upon repeated stress exposure.

摘要

应激暴露会损害大脑结构和功能,导致认知缺陷,并增加患精神疾病的风险,如抑郁症、精神分裂症、焦虑症和创伤后应激障碍。特别是,应激暴露会影响海马 CA1 的功能和结构,导致情景记忆受损。在这里,我们应用纵向深部脑光学成像来研究在应激暴露的小鼠中,活动模式的变化与背侧 CA1 锥体神经元的结构可塑性以及海马依赖的学习和记忆之间的联系。我们发现,几天的重复应激会导致神经元活动的大量增加,随后破坏了这种活动的时间结构和空间编码。然后,我们跟踪了结构兴奋性连接的动力学,作为重复应激引起的活动变化的潜在原因。因此,我们发现,重复应激会导致即刻发生的 spinogenesis 减少,随后导致棘突稳定性下降。相比之下,急性应激会导致与应激事件时间接近的棘突的稳定性增加。重要的是,活动水平、结构连接和活动模式变化之间的时间关系表明,在重复应激暴露后,结构连接的丧失介导了活性增加与时间组织和空间信息内容损伤之间的转变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bcc/9468341/2ddb634ab329/41398_2022_2107_Fig1_HTML.jpg

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