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Synapse impairment associated with enhanced apoptosis in post‐traumatic stress disorder
Author(s) -
Chen Xinzhao,
Jiang Yifan,
Wang Jiayu,
Liu Yishu,
Xiao Menglei,
Song Congshan,
Bai Yu,
Yinuo Han Nancy,
Han Fang
Publication year - 2020
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.22134
Subject(s) - neuroscience , axon , synapse , dendritic spine , synaptic pruning , dendrite (mathematics) , hippocampus , biology , prefrontal cortex , hippocampal formation , microglia , inflammation , immunology , geometry , mathematics , cognition
Abstract 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.