急性心理性应激诱发的神经内分泌反应及其影响因素

急性心理性应激源分别通过下丘脑-脑垂体-肾上腺轴(hypothalamus–pituitary–adrenal axis,HPAA)和交感神经-肾上腺髓质轴(sympathetic-adrenal medulla axis)诱发神经内分泌反应。唾液皮质醇被认为是检测急性心理性应激所诱发的HPA轴反应的稳定指标。以特里尔社会应激测试(Trier Social Stress Test,TSST)及其变式作为应激源, 以HPA轴的反应作为应激指标, 影响个体在急性心理性应激情境中发生特异性神经内分泌反应的因素主要包括人口统计学、环境和应激频率三大方面, 未来应加强急性心理性应激所诱发的神经内分泌反应的纵向研究。     

应激神经成像的研究述评

HPA轴(hypothalamic-pituitary-adrenal cortex axis)是人体的重要内分泌应激系统, 大脑通过控制HPA轴活动影响机体在应激情境中皮质醇(cortisol)的分泌, 同时皮质醇分泌对大脑也具有负反馈作用, 影响着大脑边缘系统的重塑; 海马、杏仁核、前额叶皮层和脑干都参与了应激反应中的皮质醇调节; 未来研究要进一步对应激源细化分类, 并且试图找到适合事件相关电位技术的社会心理性应激实验范式。     

人类应激内分泌轴功能状态的测量

HPA轴(下丘脑?垂体?肾上腺皮质轴, hypothalamic-pituitary-adrenal cortex axis)是人类重要的应激内分泌轴, 静息与应激条件下HPA轴的机能障碍能引发应激相关疾病, 而HPA轴机能障碍的表现和原因并不明确。皮质醇作为HPA轴的终端产物能直接反映HPA轴活动, 唾液皮质醇优于其他生物样本皮质醇的特性使其成为测量HPA轴活动的最优指标, 因此寻找到合适的唾液皮质醇标识来反映静息与应激条件下的HPA轴调节变化, 能促进理解HPA轴机能障碍与疾病间的神经内分泌通路。近来研究常用的是以皮质醇觉醒反应(cortisol -awakening response, CAR)与特里尔社会应激测试(Trier social stress test, TSST)来分别表示静息与应激条件下的HPA轴活动。未来研究将结合应激反应的生理、心理指标, 进一步考察HPA轴调节的脑网络, 为应激反应提供脑-神经内分泌通路的生物基础。     

心理行为干预对心血管活动的影响

早在本世纪初．Cannon(1936)等人的研究就已经证明：心理压力和情绪应激可使自主神经系统发生改变,从而导致心率、心输出量、血压等发生明显的变化。情绪应激一方面可以引起自主神经,尤其是交感神经的变化．从而激活交感一肾上髓质系统;另一方面,情绪应激可使下丘脑释放促肾上腺皮质激素释放因子,从而激活垂体一肾上皮质系统。心理实验研究表明,上升的交感一肾上髓质活动或垂体一肾上皮质活动与动脉硬化过程和临床冠心病的许多病理生理状态联系在一起,例如由应激引起的紧张引起交感神经水平升高,这可能是高血压形成的一个重要因素。     

神经质人格的神经生理基础

神经质作为一种人格特质, 核心特征是具有负性情绪体验的倾向。高神经质个体表现出更强的情绪反应、更差的情绪感知和应对, 因而体验到更多的负性情绪, 进而容易形成一系列精神障碍和身体疾病。因此, 神经质成为精神病理学中一个重要的风险因素。来自自主神经系统、神经内分泌系统和脑的证据发现, 高神经质个体心血管灵活性降低、HPA轴基线活动增强、EEG活动增大以及负性情绪引起的杏仁核活动增强, 其中杏仁核的自上而下和自下而上通路可能是整合多方面证据的关键。进一步研究应致力于将遗传学、电生理学、生物化学、脑成像技术等相结合, 构建神经质产生、形成的神经生理模型。     

腹式呼吸对皮肤温度影响的初步探讨

1　问题的提出　　自主神经系统分为交感神经系统和副交感神经系统 ,这两个系统交互抑制。Cannon(1936 )等人的研究已经证明 :心理压力 (stress)和情绪应激可使自主神经系统发生改变 ,从而导致心率、心输出量、血压等发生明显的变化。目前 ,随着生活节奏的加快 ,引起应激的因素越来越多 ,遭受紧张刺激在人生中是不可避免的。所以人们找出一些放松方法来应对应激引起的生理反应。腹式呼吸就是激发放松反应的有效途径之一。交感神经系统支配着血管壁的平滑肌 ,使之产生舒张和收缩 ,其兴奋性下降 ,手指血管平滑肌舒张 ,手指血流量增大 ,手温升…     

经前期综合征女性的HPA轴功能失调：一项基于皮质醇水平的元分析

HPA轴(Hypothalamic-Pituitary-Adrenal,HPA)功能失调是压力相关情绪障碍形成或者恶化的决定因素。为系统评价基线状态和面临环境挑战时经前期综合征(PremenstrualSyndrome,PMS)女性基于皮质醇水平的HPA轴功能失调,对1990年以来的32项研究(总样本量N=1280)进行了定量整合,以期为女性经前期综合征的病因和干预提供参考。结果发现：在基线研究中, PMS女性黄体期的皮质醇含量显著低于普通女性,且受到皮质醇测量时间的调节作用;PMS女性卵泡期的皮质醇含量与普通女性无显著差异。环境挑战研究的结果与基线研究类似,PMS女性黄体期的皮质醇含量显著低于普通女性,但卵泡期的皮质醇含量与普通女性无显著差异。该结果提示压力内分泌轴的持久改变和面对压力时的HPA轴反应迟钝是PMS产生的可能病理机制。未来研究应关注应激调节策略来改善PMS的不良反应。     

创伤后应激障碍患者的HPA轴功能变化的时间序列特征

已知创伤后应激障碍(posttraumatic stress disorder, PTSD)患者表现出HPA轴(hypothalamic-pituitary- adrenocortical axis)功能异常, 而皮质醇是反映PTSD患者HPA轴功能的重要生物标记。近期的研究结果提示, PTSD患者的皮质醇水平变化可能有明显的时间序列特征, 即应激事件发生后先升高, 后下降至正常水平之下。这一特征受到生物标记的时间特性, 患者病程, 应激源类型和强度, 伴生疾病等因素的干扰和掩蔽。未来研究应进一步采用长期追踪设计, 控制干扰因素的影响, 结合急性应激和慢性应激生物标记来综合验证PTSD患者皮质醇水平变化的时间序列特征|并利用该特征预测PTSD的发生、发展, 以便及时进行干预|考虑皮质醇的代谢、拮抗等机制, 结合多种生物标记综合评估、诊断PTSD患者的HPA轴功能活性。     

心理应激与心理干预

自塞里提出应激理论以来,学者们对应激引起的疾病更加重视并进行了深入研究.目前对应激反应的机理认为是当生物体受到各种刺激时,能引起下丘脑-垂体-肾上腺皮质系统功能活动增强而引起的反应.应激反应本身能够协调机体的适应力,所以有"应激无害论"一说.如果过激就会引起机体的生理、病理、心理改变.如同中医的七情学说,在正常情况下,七情是人的正常情绪反应,如果过激就会致病.     

表观遗传修饰在应激诱发抑郁症中的作用

应激可以对个体的生理和行为产生负面影响, 甚至导致抑郁症, 但病因机制尚不清楚。近年来许多研究发现应激导致的表观遗传修饰变化影响抑郁症的发生。表观遗传是指DNA序列不发生变化, 但基因表达却发生了可遗传的改变。应激引起的HPA轴、单胺类递质、BDNF三个方面的表观遗传修饰的变化, 在抑郁症发生中发挥重要作用。最后提出了目前表观遗传机制研究的局限性和未来研究热点。     

The hypothalamo-pituitary-adrenal axis in chronic fatigue syndrome and fibromyalgia syndrome

The hypothalamo-pituitary-adrenal (HPA) axis plays a major role in the regulation of responses to stress. Human stress-related disorders such as chronic fatigue syndrome (CFS), fibromyalgia syndrome (FMS), chronic pelvic pain and post-traumatic stress disorder are characterized by alterations in HPA axis activity. However, the role of the HPA axis alterations in these stress-related disorders is not clear. Most studies have shown that the HPA axis is underactive in the stress-related disorders, but contradictory results have also been reported, which may be due to the patients selected for the study, the methods used for the investigation of the HPA axis, the stage of the syndrome when the tests have been done and the interpretation of the results. There is no structural abnormality in the endocrine organs which comprise the HPA axis, thus it seems that hypocortisolemia found in the patients with stress-related disorder is functional. It may be also an adaptive response of the body to chronic stress. In this review, tests used in the assessment of HPA axis function and the HPA axis alterations found in CFS and FMS are discussed in detail.     

Evidence for discrete profiles of children’s physiological activity across three neurobiological system and their transitions over time

The conceptualization of stress‐responsive physiological systems as operating in an integrated manner is evident in several theoretical models of cross‐system functioning. However, limited empirical research has modeled the complexity of multisystem activity. Moreover few studies have explored developmentally regulated changes in multisystem activity during early childhood when plasticity is particularly pronounced. The current study used latent profile analysis (LPA) to evaluate multisystem activity during fall and spring of children's transition to kindergarten in three biological systems: the parasympathetic nervous system (PNS), sympathetic nervous system (SNS), and hypothalamic pituitary adrenal (HPA) axis. Latent transition analysis (LTA) was then used to examine the stability of profile classification across time. Across both timepoints, three distinct profiles of multisystem activity emerged. One profile was characterized by heightened HPA axis activity (HPA Axis Responders), a second profile was characterized by moderate, typically adaptive patterns across the PNS, SNS, and HPA axis (Active Copers/Mobilizers), and a third profile was characterized by heightened baseline activity, particularly in the PNS and SNS (Anticipatory Arousal/ANS Responders). LTA of fall‐to‐spring profile classifications indicated higher probabilities that children remained in the same profile over time compared to probabilities of profile changes, suggesting stability in certain patterns of cross‐system responsivity. Patterns of profile stability and change were associated with socioemotional outcomes at the end of the school year. Findings highlight the utility of LPA and LTA to detect meaningful patterns of complex multisystem physiological activity across three systems and their associations with early adjustment during an important developmental transition.     

Circadian activity of the hypothalamic-pituitary-adrenal axis is differentially affected in the rat chronic mild stress model of depression

The altered activity of the hypothalamic-pituitary-adrenal (HPA) axis is often observed in stress-related disorders. According to the literature, about 60% of patients with major depressive disorder elicit high levels of cortisol. It is still unclear why high cortisol levels are not observed in all patients. In this study, we used the chronic mild stress (CMS) rat model of depression, which is based on continuous exposure to unpredictable stressors, to track longitudinal changes in HPA function using fecal corticosterone metabolites (FCM) as a read out. The dexamethasone suppression test was used to assess negative feedback inhibition of the HPA axis. Our results show (1) a disturbance in diurnal corticosterone rhythm measured as fluctuations of the diurnal FCM peak, (2) differences in corticosterone levels between stress-susceptible and stress-resilient animals, (3) recovery of diurnal corticosterone rhythm after 8 weeks of CMS, and (4) alterations in sensitivity to dexamethasone in negative feedback regulation of corticosterone secretion during the time course of CMS. Thus, a disruption of HPA axis circadian rhythmicity coincides with the initial state in the development of depression-like behavior. This chronobiological abnormality, as well as the hypersecretion of corticosterone, is state, rather than trait, dependent.     

The neuroendocrinology of posttraumatic stress disorder: new directions

Studies of the hypothalamic-pituitary-adrenal (HPA) axis in persons with posttraumatic stress disorder (PTSD) have produced variable findings. This review focuses on the factors likely to have affected the outcome of these studies, including population characteristics and experimental design. Also discussed is a possible role for the adrenal neurosteroid dehydroepiandrosterone (DHEA) as a mediator of HPA axis adaptation to extreme stress and the psychiatric symptoms associated with PTSD. The antiglucocorticoid properties of DHEA may contribute to an upregulation of HPA axis responses as well as mitigate possible deleterious effects of high cortisol levels on the brain in some PTSD subpopulations. The neuromodulatory effects of DHEA and its metabolite DHEAS at gamma-aminobutyric acid and N-methyl-D-aspartate receptors in the brain may contribute to psychiatric symptoms associated with PTSD. The possible importance of other neurohormone systems in modulating HPA axis and symptom responses to traumatic stress is also discussed. Understanding the complex interactions of these stress-responsive neurosteroid and peptide systems may help explain the variability in patterns of HPA axis adaptation, brain changes, and psychiatric symptoms observed in PTSD and lead to better targeting of preventive and therapeutic interventions.     

Endocannabinoids and stress

Endogenous cannabinoids play an important role in the physiology and behavioral expression of stress responses. Activation of the hypothalamic-pituitary-adrenal (HPA) axis, including the release of glucocorticoids, is the fundamental hormonal response to stress. Endocannabinoid (eCB) signaling serves to maintain HPA-axis homeostasis, by buffering basal activity as well as by mediating glucocorticoid fast feedback mechanisms. Following chronic stressor exposure, eCBs are also involved in physiological and behavioral habituation processes. Behavioral consequences of stress include fear and stress-induced anxiety as well as memory formation in the context of stress, involving contextual fear conditioning and inhibitory avoidance learning. Chronic stress can also lead to depression-like symptoms. Prominent in these behavioral stress responses is the interaction between eCBs and the HPA-axis. Future directions may differentiate among eCB signaling within various brain structures/neuronal subpopulations as well as between the distinct roles of the endogenous cannabinoid ligands. Investigation into the role of the eCB system in allostatic states and recovery processes may give insight into possible therapeutic manipulations of the system in treating chronic stress-related conditions in humans.     

Adolescent Personality: Associations With Basal,Awakening, and Stress‐Induced Cortisol Responses

The purpose of the present study was to investigate the associations between personality facets and hypothalamic‐pituitary‐adrenal (HPA) axis functioning. Previous studies have mainly focussed on stress‐induced HPA‐axis activation. We hypothesized that other characteristics of HPA‐axis functioning would have a stronger association with personality based on the neuroendocrine literature. Data (n = 343) were used from the TRacking Adolescents' Individual Lives Survey (TRAILS), a large prospective cohort study of Dutch adolescents. We studied the association between facets of Neuroticism, Extraversion, and Conscientiousness and basal cortisol, the cortisol awakening response (CAR), and four measures of stress‐induced HPA‐axis activity. Basal cortisol levels were related to facets of all three personality traits. The CAR and stress‐induced cortisol were not related to personality. Possibly due to its more trait‐like nature, basal cortisol seems more informative than stress‐induced cortisol when investigating trait‐like characteristics such as personality facets.     

Involvement and role of the hypothalamo-pituitary-adrenal (HPA) stress axis in animal models of chronic pain and inflammation

Hypothalamo-pituitary-adrenal (HPA) axis changes have been reported in several disease states, including major depressive disorder, rheumatoid arthritis, multiple sclerosis and various other conditions associated with chronic pain. These observations suggest that stress and the HPA axis may play important roles in the pathology of these diseases. In order to contribute to a better understanding of the role that chronic stress may play in human pathology, this review article explores the involvement of the HPA axis in those animal models of chronic pain and inflammation that entail persistent rather than intermittent stress.     

Glutamate-mediated neuroplasticity in a limbic input to the hypothalamus

Emotionally-salient stressors are processed by cortical and limbic circuits that provide important regulatory input to the hypothalamic-pituitary-adrenal (HPA) axis. However, exposure to chronic or severe stress may cause disregulation of the axis and a variety of physiological and psychological symptoms. The mechanisms that underlie stress-induced alterations in HPA axis function are not well characterized, but one possibility is that severe stress causes plastic changes in limbic inputs to the hypothalamus. We examined plasticity within the bed nucleus of stria terminalis (BNST) and the hypothalamic paraventricular nucleus (PVN) with a stimulating electrode in the BNST and a recording electrode in the PVN. High-frequency BNST stimulation produced long-lasting suppression of evoked field potentials recorded from the PVN, and this effect was blocked by administration of MK-801. Accordingly, rapid glutamate-mediated neuroplasticity in the BNST to PVN neurocircuitry may contribute to plasticity in limbic regulation of the HPA axis.