Gilad Gad M, Gilad Varda H
Research and Development, Laboratory of Neuroscience, Assaf Harofeh Medical Center, P.O. Beer Yaakov, Zrifin 70300, Israel.
Cell Mol Neurobiol. 2003 Oct;23(4-5):637-49. doi: 10.1023/a:1025036532672.
An early transient increase in brain polyamine (PA) metabolism, termed the PA-stress-response (PSR), is a common reaction to stressful stimuli, including physical, emotional, and hormonal stressors, with a magnitude related to the stress intensity. In the extreme, traumatic injury can result in an incomplete PSR, with persistent accumulation of putrescine and eventual reduction in the concentrations of the higher polyamines (PAs), spermidine and spermine. Chronic intermittent application of stressors causes a recurrence of the brain PSR, but, in contrast, it leads to habituation of the response in the periphery (liver). Severe continuous stress, however, may lead to accumulation of brain PAs. Long-term inhibition of PA synthesis depletes brain PAs and can result in altered emotional reactivity to stressors. Furthermore, the brain PSR, in contrast to the periphery, can be blocked by a long-term, but not by short-term, treatment with lithium, the most efficacious treatment of manic-depressive illness. The brain PSR is developmentally regulated, and the switch to the mature pattern coincides with the cessation of the "stress hyporesponsive period" in the hypothalamic-pituitary-adrenocortical (HPA) system. In contrast to the brain and liver, the PSR in the adrenal and thymus is down-regulated by acute stressors. Transient up-regulation of the PSR, as in the brain and liver, is implicated in cell survival while its down-regulation is implicated in cell death. Taken together, the findings indicate that the PSR is a dynamic process that varies with the type, intensity, and duration of stressors, and implicate this response as an adaptive mechanism in the reaction to stressful events. Under persistent stressful conditions, however, the PSR may be maladaptive as may be reflected by PA accumulation. This raises the hypothesis that proper regulation of brain PSR may be critical for neuronal function and for an appropriate behavioral response to stressors.
大脑多胺(PA)代谢的早期短暂增加,即所谓的PA应激反应(PSR),是对包括身体、情绪和激素应激源在内的应激刺激的常见反应,其强度与应激强度相关。在极端情况下,创伤性损伤可导致PSR不完整,腐胺持续积累,最终导致高级多胺(PAs)、亚精胺和精胺浓度降低。慢性间歇性施加应激源会导致大脑PSR复发,但与之相反的是,它会导致外周(肝脏)反应的适应性变化。然而,严重的持续应激可能导致大脑PA积累。长期抑制PA合成会耗尽大脑PA,并可能导致对应激源的情绪反应改变。此外,与外周不同,大脑PSR可被锂长期治疗阻断,但不能被短期治疗阻断,锂是治疗躁狂抑郁症最有效的药物。大脑PSR受发育调节,向成熟模式的转变与下丘脑-垂体-肾上腺皮质(HPA)系统中“应激低反应期”的停止相吻合。与大脑和肝脏不同,肾上腺和胸腺中的PSR会被急性应激源下调。PSR的短暂上调,如在大脑和肝脏中一样,与细胞存活有关,而其下调与细胞死亡有关。综上所述,这些发现表明PSR是一个动态过程,随应激源的类型、强度和持续时间而变化,并暗示这种反应是对应激事件反应中的一种适应性机制。然而,在持续的应激条件下,PSR可能是适应不良的,这可能表现为PA积累。这就提出了一个假设,即大脑PSR的适当调节可能对神经元功能和对应激源的适当行为反应至关重要。