压力、下丘脑-垂体-肾上腺轴、下丘脑-垂体-性腺轴和攻击性。

IF 3.2 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM Metabolic brain disease Pub Date : 2024-07-31 DOI:10.1007/s11011-024-01393-w
Ngala Elvis Mbiydzenyuy, Lihle-Appiah Qulu
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引用次数: 0

摘要

这篇综合性综述探讨了下丘脑-垂体-肾上腺(HPA)轴、下丘脑-垂体-性腺(HPG)轴与攻击行为之间错综复杂的关系。本书详细概述了这些轴的生理和功能,以及对攻击行为的影响。负责应激反应的 HPA 轴在面对各种应激源时被激活,并可影响攻击行为。糖皮质激素(如皮质醇)在应激诱导的 HPA 轴激活过程中起着至关重要的作用,并与攻击倾向有关。长期应激会导致 HPA 轴失调,从而导致皮质醇水平的改变,并有可能引发攻击行为。HPG 轴,尤其是雄性激素睾酮,也与攻击行为密切相关。动物和人体研究一致表明,睾酮水平与攻击性之间存在正相关。大脑神经回路中的雄性激素受体在调节攻击行为方面起着至关重要的作用。HPA 轴和 HPG 轴之间的相互作用进一步促进了攻击行为的调节。这些轴之间的反馈机制和串扰提供了一个复杂的系统,用于调节压力和生殖功能,从而影响攻击行为。此外,应激对生殖功能的影响,特别是雄激素在应激诱导的攻击行为中的作用,也进一步增加了这种关系的复杂性。综述还讨论了临床干预的未来方向和意义。要了解攻击行为的神经生物学机制,需要综合运用分子、细胞和电路层面的方法。包括动物模型和人体研究在内的转化视角可以弥补基础研究和临床应用之间的差距。最后,本综述探讨了攻击行为相关疾病的治疗策略,强调了在全面了解 HPA 轴和 HPG 轴之间相互作用的基础上进行有针对性干预的重要性。总之,本综述全面概述了攻击行为的生理和神经生物学机制,并特别关注 HPA 轴和 HPG 轴之间的相互作用。通过阐明压力、荷尔蒙和攻击行为之间复杂的相互作用,这项研究为未来的调查和潜在的攻击相关疾病的治疗干预铺平了道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Stress, hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-gonadal axis, and aggression.

This comprehensive review explores the intricate relationship between the hypothalamic-pituitary-adrenal (HPA) axis, the hypothalamic-pituitary-gonadal (HPG) axis, and aggression. It provides a detailed overview of the physiology and functioning of these axes, as well as the implications for aggressive behavior. The HPA axis, responsible for the stress response, is activated in response to various stressors and can influence aggressive behavior. Glucocorticoids, such as cortisol, play a crucial role in stress-induced activation of the HPA axis and have been implicated in aggressive tendencies. Chronic stress can dysregulate the HPA axis, leading to alterations in cortisol levels and potentially contributing to aggressive behavior. The HPG axis, particularly the androgen hormone testosterone, is also closely linked to aggression. Animal and human studies have consistently shown a positive association between testosterone levels and aggression. The androgen receptors in the brain's neural circuitry play a critical role in modulating aggressive behavior. Interactions between the HPA and HPG axes further contribute to the regulation of aggression. Feedback mechanisms and crosstalk between these axes provide a complex system for the modulation of both stress and reproductive functions, which can impact aggressive behavior. Additionally,the influence of stress on reproductive functions, particularly the role of androgens in stress-induced aggression, adds further complexity to this relationship. The review also discusses the future directions and implications for clinical interventions. Understanding the neurobiological mechanisms underlying aggression requires integrating molecular, cellular, and circuit-level approaches. Translational perspectives, including animal models and human studies, can bridge the gap between basic research and clinical applications. Finally, therapeutic strategies for aggression-related disorders are explored, highlighting the importance of targeted interventions based on a comprehensive understanding of the interactions between the HPA and HPG axes. In conclusion, this review provides a comprehensive overview of the physiological and neurobiological mechanisms underlying aggression, with a specific focus on the interplay between the HPA and HPG axes. By elucidating the complex interactions between stress, hormones, and aggressive behavior, this research paves the way for future investigations and potential therapeutic interventions for aggression-related disorders.

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来源期刊
Metabolic brain disease
Metabolic brain disease 医学-内分泌学与代谢
CiteScore
5.90
自引率
5.60%
发文量
248
审稿时长
6-12 weeks
期刊介绍: Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.
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