基于素质-应激模型的飞行员心理健康

目的:飞行员的心理健康对于保证飞行安全、确保飞行任务的完成具有重要意义,探讨飞行员心理健康的根源,即特定的心理素质,对保障飞行安全将有重要意义。方法:主要介绍心理健康与心理素质的内涵与联系,通过分析影响心理健康的素质-应激模型,理论推导出飞行员心理健康的心理素质-应激交互作用模型,并由心理健康状态的测量佐证其合理性。结果:制约飞行员心理健康的心理素质有7个维度,21个因子。结论:心理素质是制约心理健康的内源性因素,飞行员素质-应激交互作用模型的建立对飞行员心理健康的研究有一定的参考。     

大鼠束缚-浸水应激模型体温降低与应激性胃溃疡的关系

为探讨"束缚刺激"和"冷水刺激"在束缚-浸水应激性胃溃疡形成中各自的作用及体温降低与应激性胃溃疡的关系,本研究检测了束缚-浸水应激和不同温度下单纯浸水应激对胃粘膜和腹腔温度的影响。相同水温下束缚-浸水应激和单纯浸水应激导致大鼠产生同等程度的胃溃疡,表明"冷水刺激"在束缚-浸水应激导致的胃溃疡中起重要作用,而"束缚刺激"不起重要作用。浸水的水温越低,腹腔温度就越低,胃溃疡也就越严重,说明大鼠束缚-浸水应激模型中冷水刺激引起体温降低是胃溃疡的诱发因素。     

4-苯基丁酸对创伤后应激障碍大鼠认知能力的影响

目的:观察4-苯基丁酸(4-PBA)对创伤后应激障碍(PTSD)大鼠海马神经元内质网应激(ERS)与凋亡的影响,探讨4-PBA改善PTSD大鼠认知能力的机制。方法:36只成年SD大鼠随机分为正常组、PTSD组和4-PBA+PTSD组,每组12只。PTSD组采用单次延长应激(SPS)构建PTSD大鼠模型,4-PBA+PTSD组从造模次日开始每天于固定时间腹腔注射4-PBA(40 mg/kg),连续给药7 d。Morris水迷宫实验检测各组大鼠的学习记忆能力; Western Blot实验检测各组大鼠海马葡萄糖调节蛋白78(GRP78)、CCAAT增强子结合蛋白同源蛋白(CHOP)及B淋巴细胞瘤-2(Bcl-2)、蛋白激酶R样内质网激酶(PERK)-真核翻译起始因子2α(e IF2α)-活化转录因子4(ATF4)信号通路相关蛋白表达的变化。结果:在Morris水迷宫实验中,与对照组比较,PTSD组大鼠学习记忆能力明显减退(P 0.01);与PTSD组比较,4-PBA+PTSD组大鼠学习记忆功能明显改善(P 0.01)。Western Blot实验结果显示,与对照组比较,PTSD组大鼠GRP78、CHOP的表达明显增加(P 0.01),Bcl-2的表达显著减少(P 0.01),PERK、e IF2α、p-eIF2α表达显著增加(P 0.05),与PTSD组比较,4-PBA+PTSD组大鼠GRP78、CHOP的表达明显减少(P 0.01),Bcl-2的表达显著增加(P 0.05),PERK、e IF2α、p-eIF2α表达显著减少(P 0.05)。结论:4-PBA能够通过激活PERK-eIF2α-ATF4信号通路抑制PTSD大鼠海马神经元的ERS和凋亡,进而改善PTSD大鼠的认知能力。     

军事应激下军人血清细胞因子与皮质醇水平含量分析

等级战备状态下高强度的应激训练、战前形势教育、紧张气氛的体验等 ,对和平年代的军人无疑都是极大的生理、心理应激。本文以等级战备状态为应激源 ,旨在探讨军事应激下军人免疫功能和血清皮质醇变化 ,为研究部队军事生活应激源提供背景资料。对象　研究组 :2 0 0 1年 10月间某集团军进入三级战备状态的应激分队军人 45名 ,男性 ,年龄 18-2 9岁 ,平均2 1± 3岁 ,军龄 1-13年 ,文化程度 ,初中 2 0人 ,高中 18人 ,大专以上 7人。干部 6人 ,战士 3 9人。对照组选择平时状态的军人 3 0人 ,男性 ,平均 2 1± 3岁 ,两组在文化、职务、性别、环境…     

心理应激雌性大鼠海马-下丘脑-垂体雌激素受体的变化

目的：探讨雌性大鼠心理应激状态下，海马-下丘脑-垂体雌激素受体（ER）的改变，进而阐明卵巢内分泌功能失调的机制。 方法: 采用声-光-电复合刺激作为心理应激制造大鼠卵巢内分泌功能失调模型；采用免疫组化方法和图像分析仪定量分析海马-下丘脑-垂体ER的表达。 结果： 采用声-光-电复合刺激雌性大鼠后，大鼠海马-下丘脑-垂体ER的表达下降。 结论： 心理应激雌性大鼠海马-下丘脑-垂体ER下降可能是卵巢内分泌功能失调的机制之一。     

急性应激对大鼠行为学及蓝斑TH、DBH基因表达的影响

目的观察急性应激状态下大鼠行为学的改变及不同时间点蓝斑内酪氨酸羟化酶（TH）和多巴胺-β-羟化酶（DBH）的基因表达。方法将24只健康雄性Wistar大鼠随机分为空白对照组和模型组,模型组又分为造模后1、3、6h组,每组6只。运用束缚和游泳的方法造模,观察其行为学的改变;并分别在造模后相应时间点取出蓝斑,用RT-PCR法检测蓝斑TH、DBH的表达。结果模型组造模前后比较,1、6h组的穿越格数和直立次数明显下降（P〈0.05）,3h组的穿越格数、直立次数和理毛次数均明显降低（P〈0.05,P〈0.05,P〈0.01）;与对照组大鼠相比,造模后1h组的穿越格数减少（P〈0.05）,1、3h组的直立次数明显降低（P〈0.01,P〈0.05）,1、3、6h组的理毛次数降低明显且差异均有统计学意义（均P〈0.01）。模型组蓝斑TH和DBH表达水平较对照组升高,其中3h组表达最高（P〈0.05）,1、6h组差异均无统计学意义（P〉0.05）,TH和DBH两者的表达趋势相似。结论急性应激使大鼠的行为能力降低,蓝斑去甲肾上腺素能神经元中TH、DBH表达增高,使去甲肾上腺素合成增多,而去甲肾上腺素可以显著影响大鼠的情绪行为,在应激过程中起重要作用;TH、DBH表达的增高可能参与了急性应激所致的行为异常。     

慢性应激对小鼠心理行为及血清IFN-γ、IL-4水平的影响

目的探讨慢性应激对小鼠情绪行为以及血清IFN-γ、IL-4水平的影响。方法选取BALB/c小鼠50只,随机分为正常对照组和应激组,每组25只。采用自制的束缚制动方法建立慢性心理应激模型,应激后进行旷场实验和悬尾实验,摘眼球取血采用ELISA方法检测血清IFN-γ和IL-4的水平。结果应激组小鼠在旷场实验中的中央格停留时间显著延长(P0.01),探究活动显著减少(P0.01),粪便次数显著增多(P0.01);悬尾实验中,应激组小鼠不动时间显著延长(P0.01);应激组小鼠血清IFN-γ水平明显低于对照组(P0.05),IL-4水平与对照组相比差异无统计学意义(P0.05)。结论慢性心理应激可以导致机体行为发生改变,出现焦虑、抑郁情绪,同时降低机体的免疫功能。     

连续单一应激后大鼠海马5-HT_(1A)受体活性与糖皮质激素受体表达的关系

目的:观察连续单一应激(SPS)大鼠海马糖皮质激素受体(GR)变化与5-HT1A受体的关系,探讨创伤后应激障碍的发病机制。方法:选用雄性成年Wistar大鼠45只,将大鼠随机分为对照组、模型组和阻断组,每组15只。模型组和阻断组给予SPS应激,其中阻断组大鼠在接受SPS前用55-HT1A受体阻断剂WAY100635预处理。采用免疫组织化学和免疫印迹技术测定海马GR水平,采用逆转录-聚合酶链式反应检测GRmRNA表达变化。结果:(1)免疫组织化学结果显示,模型组大鼠海马GR表达高于对照组(P0.01),阻断组则低于模型组(P0.05);(2)WesternBlot结果显示,模型组大鼠海马GR相对表达高于对照组(P0.01),阻断组低于模型组(P0.01);(3)RT-PCR结果表明,与对照组比较,模型组大鼠海马GRmRNA表达增强(P0.01);与模型组比较,阻断组表达量降低(P0.05)。结论:SPS海马GR表达变化与5-HT1A受体有关。     

“脆弱性”还是“可塑性”:差别易感性模型

素质-应激模型认为,部分个体具有与生俱来的"脆弱性"素质,比他人更易受到消极环境的负面影响。差别易感性模型却认为,一部分人是具有更高的发展"可塑性"而不是脆弱性,他们比其他人不仅更易受到不利环境的消极影响,也更易受到积极的、支持性环境的有利影响。首先,对比分析了素质-应激模型和差别易感性模型的基本观点;其次,论述差别易感性模型的理论基础和相关的实证研究;最后,讨论了差别易感性模型的已有研究存在的问题和未来研究的方向。     

β-内啡肽、甲状腺激素和皮质醇在军事应激时的变化

以实弹射击考核为应激源,研究新战士受到军事应激时体内应激激素的变化.42名男性新战士,以其考核前半个月平静状态下抽血为对照组,实弹射击考核就地抽血为应激组.利用放射免疫分析法(RIA)分别对β-内啡肽(β-EP)、甲状腺激素(T3、T4)、皮质醇(COR)进行测定.结果表明,应激时,β-EP、COR明显升高(P＜0.01,P＜0.001);T3偏低,与对照组比较差异显著(P＜0.01);T4虽有升高,但无统计学意义(P＞0.05).这提示军事应激时会导致体内应激激素含量的变化,因此建立应激激素的检测,对于提高部队军事应激能力,保障指战员的身心健康是有一定价值的.     

Modification of prenatal stress effects in rats by dexamethasone and adrenocorticotrophin.

To determine if effects of prenatal stress on offspring are mediated by the maternal pituitary-adrenocortical (PAC) system, female rats were stressed during gestation while manipulating their PAC output and the growth and behavior of their offspring examined. Specifically, females were injected with ACTH, dexamethasone (DEX), or saline (SAL) during pregnancy or were untreated (CON). Half the females in each group received daily electric shock sessions from Day 7 to Day 21 of gestation. Significantly more females in the ACTH and SAL groups delivered their litters late. Although DEX produced a significant reduction in birth and weaning weights of offspring whereas ACTH did not, both DEX and ACTH blocked the increase in birth weights produced by prenatal stress in offspring of SAL treated females. However, the significant effect of stress on mortality from birth to weaning was potentiated by ACTH and mortality was increased by either DEX or ACTH alone (compared to SAL). In addition, ACTH reversed the effect of stress on open-field activity of 86–96 day old offspring: stress reduced activity of SAL offspring but increased that of ACTH offspring. DEX itself significantly increased activity of female, but not male, offspring and ACTH significantly decreased activity of unstressed offspring of both sexes. Open-field behavior of 32–38 day offspring and active and passive avoidance conditioning of 86–96 day offspring were unaffected by prenatal drug or stress treatments. Attenuation of the maternal PAC response to stress consistently blocks the effects of prenatal stress on birth weights of offspring but can potentiate, reverse, or fail to modify the effects of stress on behavior. It thus seems unlikely that prenatal stress effects on offspring behavior are mediated by the maternal PAC system.     

Physical exercise during pregnancy minimizes PTZ-induced behavioral manifestations in prenatally stressed offspring

Stress during gestation has been shown to affect susceptibility and intensity of seizures in offspring. Environmental stimuli, such as maternal physical exercise, have shown to be beneficial for brain development. Although studies have demonstrated the deleterious influence of stress during pregnancy on seizure manifestation in offspring, very little is known on how to minimize these effects. This study verified whether physical exercise during the pregnancy associated with prenatal stress minimizes seizure susceptibility in offspring at the beginning of postnatal development. Pregnant rats and male pups were divided into the following groups: control, stress, stress/forced exercise, and stress/voluntary exercise. Behavioral manifestations were analyzed after injection of pentylenetetrazol (PTZ; 45 and 60 mg/kg) at ages P15 and P25. Increased behavioral manifestations and seizure severity was observed in the stress group compared with the control group at both ages. At the dose of 45 mg/kg, offspring of stressed mothers who performed both physical exercise models showed an increase in latency for the first manifestation and decrease in the seizures severity at both ages compared with the mothers groups who were only stressed. Prenatal restraint stress potentiated PTZ-induced seizure behavior, and both forced and voluntary exercise during gestation attenuates the negative effects of PTZ-induced offspring.     

Neurodevelopmental consequences of maternal distress: what do we really know?

Schuurmans C, Kurrasch DM. Neurodevelopmental consequences of maternal distress: what do we really know? A simple internet search of ‘maternal stress and pregnancy’ turns up hundreds of hits explaining that an adverse intrauterine environment can affect fetal development and potentially lead to various learning, behavioral, and mood disorders in childhood, as well as complex diseases such as obesity and cardiovascular conditions later in life. Indeed, a growing body of literature now links several intrauterine challenges, including maternal obesity and stress, with adverse developmental outcomes in the child. Over the past 5 years, nearly 5000 publications have explored the consequences of maternal distress on young offspring, a marked increase from the 475 published studies over a comparable period 20 years ago. Yet, despite this explosion of research and widespread warnings to pregnant mothers, we still lack a basic understanding of the pathophysiology linking adverse maternal health to the onset of disease in the child, especially regarding how prenatal and perinatal challenges might affect brain development. Recent studies have begun to explore the cellular basis of the abnormal brain cytoarchitecture associated with fetal exposure to intrauterine challenges. Here, our goal is to review the scientific evidence that maternal distress interferes with key neurodevelopmental steps, as an entry point toward mapping the pathophysiology of pre‐ and perinatal stress on the unborn child's brain.     

Effects of maternal prenatal stress on offspring development: a commentary

Pregnancy is associated with major physiological changes and adaptation to these changes is crucial for normal fetal development. Heightened emotional stress during pregnancy may interfere with the necessary adaptation and lead to dysregulation of the two major stress response systems: the Hypothalamic-Pituitary-Adrenal (HPA) Axis and the Autonomic Nervous System (ANS). Negative effects on the fetus of such maladaptation have been documented in both animals and humans and range from poor birth outcomes to negative impacts on neurodevelopment, as well as long term emotional and behavioural disturbances. Conversely, it has been hypothesized that low levels of maternal prenatal stress may actually have an adaptive value for the offspring. Investigation of these associations employing physiological markers and repeated measures throughout pregnancy and postpartum of both the mother and the offspring, is required in order to understand the various effects of prenatal stress on the development of the offspring. It is also crucial to explore the possibility of variable periods of vulnerability throughout gestation. The aim of this commentary is to reexamine the current literature on the ill-effects of maternal stress during pregnancy on the offspring and to explore avenues for future treatment and prevention.     

Inherent maternal type 2 immunity: Consequences for maternal and offspring health

An inherent elevation in type 2 immunity is a feature of maternal and offspring immune systems. This has diverse implications for maternal and offspring biology including influencing success of pregnancy, offspring immune development and maternal and offspring ability to control infection and diseases such as allergies. In this review we provide a broad insight into how this immunological feature of pregnancy and early life impacts both maternal and offspring biology. We also suggest how understanding of this axis of immune influence is and may be utilised to improve maternal and offspring health.     

Maternal prenatal cortisol and the interaction of income and pre-pregnancy body mass index are independently associated with newborn cortisol

While extensive research has supported the developmental programming hypothesis regarding contributions of prenatal psychosocial or nutritional adversity to offspring stress physiology, fewer studies consider both exposures together with maternal stress physiology. This study examined newborn cortisol output during a stressor as a function of maternal pre-pregnancy health status and nutritional history (pre-pregnancy body mass index [PPBMI]), economic resources (household income), and maternal cortisol awakening response (mCAR) in late pregnancy. Participants were 102 mother-infant pairs from an economically and racial/ethnically diverse sample. Offspring salivary cortisol response to a neurobehavioral exam was assessed at 1 month. Income and maternal PPBMI were positively associated with mCAR in late pregnancy. mCAR was positively related to 1-month newborn cortisol response. The interaction of income and PPBMI was positively associated with newborn cortisol output during an exam at 1-month. Mothers with the highest PPBMI and lowest income had offspring with higher cortisol responses than offspring of mothers with higher income and lower PPBMI. There was no evidence of indirect mediation effects of predictors (PPBMI, income, and interaction) on infant cortisol via mCAR. The differential effects of the interaction of PPBMI and income suggest that these exposures influence infant cortisol output in the context of one another, independent of maternal pregnancy cortisol.     

Maternal stress and high-fat diet effect on maternal behavior, milk composition, and pup ingestive behavior

Chronic variable prenatal stress or maternal high-fat diet results in offspring that are significantly heavier by the end of the first postnatal week with increased adiposity by weaning. It is unclear, however, what role maternal care and diet play in the ontogenesis of this phenotype and what contributions come from differences already established in the rat pups. In the present studies, we examined maternal behavior and milk composition as well as offspring ingestive behavior. Our aim was to better understand the development of the obese phenotype in offspring from dams subjected to prenatal stress and/or fed a high-fat (HF) diet during gestation and lactation. We found that dams maintained on a HF diet through gestation and lactation spent significantly more time nursing their pups during the first postnatal week. In addition, offspring of prenatal stress dams consumed more milk at postnatal day (PND) 3 and offspring of HF dams consume more milk on PND 7 in an independent ingestion test. Milk from HF dams showed a significant increase in fat content from PND 10-21. Together these results suggest that gestational dietary or stress manipulations can alter the rat offspring's developmental environment, evidence of which is apparent by PND 3. Alterations in maternal care, milk composition, and pup consumption during the early postnatal period may contribute to long-term changes in body weight and adiposity induced by maternal prenatal stress or high-fat diet.     

Prenatal stress affects the rate of sexual maturation and attractiveness in bank voles

Field studies reveal that bank vole females' mobility and aggression increase during pregnancy. Here we investigated the reaction of pregnant females to social stress evoked by short but frequent meetings with another female at the same stage of pregnancy. The stress neither evoked pregnancy termination nor affected pregnancy duration but had a long-term effect on the reproductive activity of the offspring. Prenatal stress reduced the rate of sexual maturation of voles as estimated at the age of 20 days. Uterine weights of prenatally stressed females and testes weights of prenatally stressed males were significantly lower than in offspring born to nonstressed mothers. Olfactory signals are known to be important in the sexual preferences of bank voles. Adult prenatally stressed females were more attractive to other adult females than were nonstressed animals. For bank vole males, however, prenatal stress decreased the attractiveness of females; adult males selected nonstressed females over stressed partners, by odor. This study shows that prenatal conditions evoked by short but frequent encounters with another pregnant female lead to delayed puberty in females and males, and decrease sexual attractiveness in adult offspring. These two negative effects may significantly limit the reproduction of prenatally stressed offspring.     

Impact of prenatal stress on long term body weight is dependent on timing and maternal sensitivity

Stress experienced during pregnancy increases the risk for altered birth weights. Recent studies have revealed a link between abnormal birth weights and a future predisposition toward developing overweight or obesity. To determine the gestational time window when stress exposure produces the greatest impact on offspring body weight regulation, we have examined the birth weights and long-term body weight changes in offspring exposed to chronic variable stress (CVS) early, mid-, or late in gestation. As it is likely that the influences of prenatal stress on development stem from a complex interaction between both environmental and genetic factors, our study has included comparisons with offspring born to stress-sensitive (corticotropin-releasing factor receptor-2 deficient) mice. Stress experienced late in pregnancy significantly elevated offspring birth weights in wild type mice compared to unstressed controls. However, this weight difference diminished postnatally. In contrast, stress experienced mid- to late in pregnancy produced significant and long-term effects on body weight in offspring from stress-sensitive dams, were the male offspring were 15% heavier as adults. Adult offspring plasma glucose and leptin levels were also dependent on the timing of stress exposure, indicating that alterations in energy homeostasis may be influencing long-term body weight. Results from these studies support our hypothesis that the ultimate effect of prenatal stress on offspring long-term outcome is dependent on the timing of exposure and maternal sensitivity.     

Maternal and infantile influences upon exploratory behavior and emotional reactivity in the albino rat

A 2 × 2 × 2 factorial experiment was conducted to investigate the combined effects of maternal infantile handling, maternal pregnancy (offspring pre-natal) stress, and offspring infantile handling on adult open-field behavior and weight of albino rats. The primary results are as follows: (1) both offspring infantile handling and maternal pregnancy stress tend to increase adult exploratory behavior; (2) adult weight was lower for subjects whose mother had undergone stress during pregnancy than for offspring of non-stress females; (3) several 2-way interactions were found to significantly influence open-field exploration; (4) when offspring infantile handling was combined with maternal pregnancy stress, emotional reactivity (i.e., defecation) was found to increase significantly over that following either type of stimulation alone.