Synapse impairment is associated with post-traumatic stress disorder (PTSD), which is characterized by enhanced apoptosis in the hippocampus, amygdala, and other brain regions. However, there are no detailed studies on the relationship between apoptosis and synaptic connectivity in PTSD. In this review, we discuss results from various studies describing the synaptic changes observed in the PTSD brain. A decreased number of dendrites/spines or increased number of immature spines in the hippocampus, medial prefrontal cortex, and other brain regions has been reported. Studies on axon guidance, myelination, and the cytoskeleton suggest that PTSD may involve axon overgrowth and overbranching. Apoptosis affects synapse formation; low levels of caspase maintain the balance between growth cone attraction and repulsion and inhibit axon elongation. PTSD enhances neuronal apoptosis through caspase activation, which disrupts the balance between growth cone attraction and repulsion and alters growth cone trajectory, leading to axon mistargeting. Meanwhile, caspase activation induces dendritic pruning and dendrite degeneration. These events contribute to the formation of fewer and aberrant synapses, which is associated with enhanced apoptosis in PTSD.

中文翻译：

---

与创伤后应激障碍中细胞凋亡增强相关的突触损伤。

突触损伤与创伤后应激障碍 (PTSD) 相关，其特征是海马、杏仁核和其他大脑区域的细胞凋亡增强。然而，没有关于 PTSD 中细胞凋亡与突触连接之间关系的详细研究。在这篇综述中，我们讨论了各种研究的结果，这些研究描述了在 PTSD 大脑中观察到的突触变化。据报道，海马体、内侧前额叶皮层和其他大脑区域中树突/刺的数量减少或未成熟刺的数量增加。对轴突导向、髓鞘形成和细胞骨架的研究表明，PTSD 可能涉及轴突过度生长和过度分支。细胞凋亡影响突触形成；低水平的半胱天冬酶维持生长锥吸引和排斥之间的平衡并抑制轴突伸长。PTSD 通过半胱天冬酶激活增强神经元凋亡，这会破坏生长锥吸引和排斥之间的平衡并改变生长锥轨迹，导致轴突定位错误。同时，半胱天冬酶激活诱导树突修剪和树突退化。这些事件有助于形成更少和异常的突触，这与 PTSD 中的细胞凋亡增强有关。