Journal of Multiscale Neuroscience

Ying Zhou, H. Tuckwell, N. Penington
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Abstract

Stress alters neuroendocrine, autonomic, and behavioral processes to cope well with perceived threats that compromise subjective wellbeing. Just as the perception of risk can change the structure and function of brain circuitry, which may result in enduring behavioral changes. There needs to be a greater understanding of how the brain reacts to stress-related disorders and discern how the adaptation mechanisms of the central nervous system under acute stress, as well as how stress-induced adaptation mechanisms are altered under chronic stress conditions that may induce plasticity-related changes in the brain. During this interaction, the brain becomes more capable of resolving stress in a way that is either adaptive or maladaptive, leaving the most critical deficit in the emotion regulation associated with risk for pathological conditions. The essence of this associated risk involves the reciprocal influence between hypothalamic-pituitary-adrenal function, the relay nucleus within the amygdala reactivation, and the hippocampus as essential structures associated with the forebrain pathways mediating stress-induced hormones, and the gamma-aminobutyric acid neurotransmitter system as key mechanisms of regulating stress. Understanding how related emotional experiences occur on the neural level and their impact on cognition and behavior entail tracing the interaction between the hypothalamic-pituitary-adrenal axis, the hormones released by these structures, and the neuroendocrine system's reactivity to stress. The interaction between threat-sensitive brain circuitry and the neuroendocrine stress system is crucial to understanding how related emotions arise on the neural level and their impact on cognition and behavior. The hypothalamic-pituitary-adrenal axis is critical in regulating the synthesis and release of endocrine hormones through its interactions with these structures, collectively referred to as the stress response. The stress system is described in its anatomy and physiology and connections to other brain areas and endocrine systems. We explore the current evidence linking stress with pathophysiologic mechanisms implicated in stressful conditions affecting the neuronal circuitry between endocrine, metabolic, gastrointestinal, and immune systems. Examining the biopsychological contributions provides a conceptual framework for understanding the emergence of emotions and stress-related behaviors.
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多尺度神经科学杂志
压力会改变神经内分泌、自主神经和行为过程,从而更好地应对损害主观幸福感的感知威胁。正如对风险的感知可以改变大脑回路的结构和功能,这可能导致持久的行为改变。我们需要更好地了解大脑对压力相关疾病的反应,以及中枢神经系统在急性压力下的适应机制,以及压力诱导的适应机制在慢性压力条件下是如何改变的,这可能会导致大脑中可塑性相关的变化。在这种相互作用中,大脑变得更有能力以一种适应或不适应的方式解决压力,在与病理状况风险相关的情绪调节中留下最关键的缺陷。这种相关风险的本质涉及下丘脑-垂体-肾上腺功能、杏仁核再激活内的中继核和海马之间的相互影响,海马是与前脑通路介导应激诱导激素相关的基本结构,而γ -氨基丁酸神经递质系统是调节应激的关键机制。要了解相关的情绪体验是如何在神经层面上发生的,以及它们对认知和行为的影响,需要追踪下丘脑-垂体-肾上腺轴、这些结构释放的激素和神经内分泌系统对压力的反应之间的相互作用。威胁敏感脑回路和神经内分泌应激系统之间的相互作用对于理解相关情绪如何在神经水平上产生及其对认知和行为的影响至关重要。下丘脑-垂体-肾上腺轴通过与这些结构的相互作用,在调节内分泌激素的合成和释放方面至关重要,这些结构统称为应激反应。应激系统在解剖学和生理学以及与其他脑区和内分泌系统的联系中被描述。我们探索了当前的证据将应激与病理生理机制联系起来,这些机制涉及应激条件影响内分泌、代谢、胃肠道和免疫系统之间的神经回路。检查生物心理学的贡献为理解情绪和压力相关行为的出现提供了一个概念框架。
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