产科应激事件对产后抑郁症患者神经内分泌功能的影响

目的探讨产科应激事件对产后抑郁症患者神经内分泌功能的影响。方法选取我院2012-01—2014-01收治的250例妊娠足月分娩产妇,将出现产科应激事件的患者设为观察组,并随机分成A、B、C、D、E 5组,每组各50例,对应出现的产科应激事件分别为1种、2种、3种、4种、5种。选择同期50例无产科应激反应发生的产妇作为正常对照组,对比各组患者神经内分泌水平及抑郁情况。结果观察组产妇抑郁量表(EPDS)评分、血清促肾上腺皮质激素释放激素(CRH)、促肾上腺皮质激素(ACTH)、皮质醇水平显著高于对照组,差异有统计学意义(P0.05),血浆多巴胺(DA)、去甲肾上腺素(NE)、5-羟色胺(5-HT)水平显著低于对照组,差异有统计学意义(P0.05)。这种差异随着应激事件种类的增加越发明显。结论产科应激事件会对患者的神经内分泌功能造成严重的影响,患者下丘脑-脑垂体-肾上腺轴的轴功能变得亢进,致使产妇的神经内分泌失调,是产妇产后出现抑郁症状的主要原因。     

跳伞应激对空降兵新兵心理和免疫、神经内分泌的影响

目的探讨跳伞训练对空降兵新兵心理和免疫、神经内分泌指标的影响。方法选取参加跳伞空降兵146名,采用放射免疫方法检测参演跳伞前后血清皮质醇、醛固酮、促肾上腺皮质激素及免疫指标:IL-2、IL-6、IL-8水平,应用焦虑自评量表(SAS)调查,将血清学检测结果与空降兵SAS分值进行相关性分析。结果跳伞后血清COR、ALD、ACTH均升高,与跳伞前比较差异有统计学意义(P<0.05),SAS分值>50的空降兵新兵血清皮质醇和醛固酮升高更明显(P<0.05);跳伞应激后血清IL-2降低,IL-6、IL-8升高,与跳伞前比较差异有统计学意义(P<0.05),SAS分值>50的空降兵(n=25)IL-2降低和IL-6、IL-8升高更明显(P<0.05)。结论空降兵的跳伞应激可引起内分泌激素水平的改变,并对免疫系统产生一定的抑制作用。     

精神神经内分泌免疫调节的研究进展

精神神经活动损毁中枢神经系统某些部位可影响机体免疫功能,外周自主神经与免疫系统之间存在直接联系。神经递质和内分泌激素通过免疫细胞上的相应受体调节其功能,免疫细胞可直接产生神经内分泌激素或通过细胞因子影响神经内分泌系统活动,免疫系统与神经内分泌系统共同维持机体稳定。     

抗精神病药对神经内分泌的影响

传统抗精神病药 (ＡＰＤ)对精神分裂症患者神经内分泌的副作用 ,不仅给患者带来很大痛苦 ,而且也是治疗依从性差的主要原因之一。而ＡＰＤ对不同性别精神分裂症患者的影响 ,一直是人们关注的问题。对此 ,我们就有关内容进行综述。一、性激素对精神分裂症的影响据报道 ,与男性相比 ,女性精神分裂症患者有如下特点 :起病晚、阴性症状少、病程相对良性、药物疗效好及家族发病率高[1] 。这些性别差异 ,主要是由于各种性激素尤其是雌激素 (Ｅ)作用的影响。Ｍａｇｈａｒｉｏｕｓ等[1] 通过复习文献提出 ,性激素以两种方式对精神分裂症的性别差异产…     

广泛性焦虑障碍的神经生化和内分泌研究进展

本文对广泛性焦虑障碍的神经生化和神经内分泌改变进行综述。     

广泛性焦虑障碍的神经生化和内分泌研究进展

本文对广泛性焦虑障碍的神经生化和神经内分泌改变进行综述。     

强迫症的神经内分泌研究

对探讨强迫症患者的下丘脑－垂体－肾上腺皮质系统的功能状态及强迫症与抑郁症的生物联系，作者对３０例未服药的强迫症患者的基础血浆皮质醇、地塞米松抑制试验（ＤＳＴ）及氯丙咪嗪治疗前后的血催乳素含量进行测定，并以２０例健康志愿者的血浆皮质醇、ＤＳＴ和血催乳素测定值作对照。结果显示：强迫症患者基础血浆皮质醇和基础血催乳素含量高于对照组，但ＤＳＴ无一例呈脱抑制反庆；患者经氯丙咪嗪治疗后，血浆催乳素含量明显升高     

ECT后神经内分泌的变化

近十几年,国外许多研究者用不同方法对ECT治疗引起的神经内分泌变化进行了大量的研究,并提出了若干假设。本文扼要介绍这方面的研究及结果。     

利培酮对女性精神分裂症患者神经内分泌的影响

目的 探讨利培酮对女性精神分裂症患者神经内分泌的影响。方法 对58例女性精神分裂症患者存利培酮治疗至少6个月后,检测性激素水平及利培酮血药浓度。并与30名健康女性进行对照分析。结果 研究组催乳素(PRL)、睾酮水平均显著高于对照组(P<0.01),而雌二醇、孕酮水平则显著低于对照组(P<0.01)。溢乳组PRL水平显著高于无溢乳组(P<0.01),ROC曲线显示,当PRL≥98.0μg/L时溢乳的危险性升高。结论 ①利培酮治疗后可见血催乳素、睾酮水平升高,雌二醇、孕酮水平降低;②催乳素≥98.0μg/L时发生溢乳的危险性升高。探讨利培酮对神经内分泌的影响还需进一步做前瞻性研究。     

The effects of prenatal stress on expression of p38 MAPK in offspring hippocampus

The hippocampus, which has the highest density of GC receptors in the brain, is involved in the regulation of the HPA and the behavioral responses to stress. Overexposure to corticosteroid hormones is harmful to hippocampal neuron integrity. Our purpose is to investigate the effects of prenatal stress (PNS) on expression of p38 mitogen-activated protein kinase (p38 MAPK) in offspring hippocampal neurons using Western blotting and Immunohistochemistry. The prenatal restraint stress induces significant increase in the expression of p-p38 MAPK and total p38 MAPK in female offspring hippocampus. The level of p-p38 MAPK in PNS female offspring rats was significantly increased (126.41+/-3.937, n=6) compared with that in the control female offspring rats (101.35+/-3.468, n=6, P<0.01). Immunoblot analysis revealed there was significant difference in the level of total p38 MAPK between the female control and prenatal restraint stress offspring rats (101.70+/-3.162 vs. 128.111+/-2.724, respectively, P<0.01). Immunodensity of p38 MAPK was significantly increased above female control in PNS female offspring hippocampal CA3 and CA4 fields (P<0.001 vs. control group, CON). The data suggest that exposure of animals to a period of stressful experience during a critical phase could impose lasting effects on the offspring hippocampal neurons cellular signalling of offspring hippocampus.     

Sex and region difference of the expression of ERK in prenatal stress offspring hippocampus

Prenatal stress is known to cause neuronal loss and oxidative damage in the hippocampus of offspring rats. The underlying molecular mechanism has not been fully understood. The extracellularsignal-regulated kinase (ERK1/2) is recruited when the brain undergoes synaptic plasticity and remodeling. In the present study, we used Western blotting and immunohistochemistry techniques to examine the effects of prenatal restraint stress (PNS) on the expression of phosphorylated ERK (p-ERK) and total ERK. Pregnant rats in the PNS group were exposed to restraint stress on day 14-20 of pregnancy three times daily for 45min. One-month-old offspring rats were used in this experiment. PNS treatment increased the expression of p-ERK2 compared to that in the control female offspring rats and total ERK2 in female offspring hippocampus compared with that of control group. No significant changes in the amounts of total ERK1 of prenatally offspring hippocampus were observed in both genders compared with control animals. ERK immunodensity was significantly increased in PNS groups in CA3 field in male offspring hippocampus compared with control animals. ERK optical density was significantly increased in PNS female offspring hippocampus CA1, CA3 and CA4 region. However, ERK optical density was not significantly different between male control and PNS groups in CA1, CA4 fields and DG in offspring hippocampus. These findings suggest the sex and region-dependent effects of prenatal stress on the expression of ERK in offspring hippocampus. ERK expression changes induced by prenatal stress may contribute to hippocampus synaptic plasticity changes of the offspring.     

Influence of low level maternal Pb exposure and prenatal stress on offspring stress challenge responsivity

We previously demonstrated potentiated effects of maternal Pb exposure producing blood Pb(PbB) levels averaging 39 μg/dl combined with prenatal restraint stress (PS) on stress challenge responsivity of female offspring as adults. The present study sought to determine if: (1) such interactions occurred at lower PbBs, (2) exhibited gender specificity, and (3) corticosterone and neurochemical changes contributed to behavioral outcomes. Rat dams were exposed to 0, 50 or 150 ppm Pb acetate drinking water solutions from 2 mos prior to breeding through lactation (pup exposure ended at weaning; mean PbBs of dams at weaning were <1, 11 and 31 μg/dl, respectively); a subset in each Pb group underwent prenatal restraint stress (PS) on gestational days 16–17. The effects of variable intermittent stress challenge (restraint, cold, novelty) on Fixed Interval (FI) schedule controlled behavior and corticosterone were examined in offspring when they were adults. Corticosterone changes were also measured in non-behaviorally tested (NFI) littermates. PS alone was associated with FI rate suppression in females and FI rate enhancement in males; Pb exposure blunted these effects in both genders, particularly following restraint stress. PS alone produced modest corticosterone elevation following restraint stress in adult females, but robust enhancements in males following all challenges. Pb exposure blunted these corticosterone changes in females, but further enhanced levels in males. Pb-associated changes showed linear concentration dependence in females, but non-linearity in males, with stronger or selective changes at 50 ppm. Statistically, FI performance was associated with corticosterone changes in females, but with frontal cortical dopaminergic and serotonergic changes in males. Corticosterone changes differed markedly in FI vs. NFI groups in both genders, demonstrating a critical role for behavioral history and raising caution about extrapolating biochemical markers across such conditions. These findings demonstrate that maternal Pb interacts with prenatal stress to further modify both behavioral and corticosterone responses to stress challenge, thereby suggesting that studies of Pb in isolation from other disease risk factors will not reveal the extent of its adverse effects. These findings also underscore the critical need to extend screening programs for elevated Pb exposure, now restricted to young children, to pregnant, at risk, women.     

Duloxetine prevents the effects of prenatal stress on depressive-like and anxiety-like behavior and hippocampal expression of pro-inflammatory cytokines in adult male offspring rats

Stress during pregnancy may cause neurodevelopmental and psychiatric disorders. However, the mechanisms are largely unknown. Currently, pro-inflammatory cytokines have been identified as a risk factor for depression and anxiety disorder. Unfortunately, there is very little research on the long-term effects of prenatal stress on the neuroinflammatory system of offspring. Moreover, the relationship between antidepressant treatment and cytokines in the central nervous system, especially in the hippocampus, an important emotion modulation center, is unclear. Therefore, the aim of this study was to determine the effects of prenatal chronic mild stress during development on affective-like behaviors and hippocampal cytokines in adult offspring, and to verify whether antidepressant (duloxetine) administration from early adulthood could prevent the harmful consequences. To do so, prenatally stressed and non-stressed Sprague-Dawley rats were treated with either duloxetine (10 mg/kg/day) or vehicle from postnatal day 60 for 21 days. Adult offspring were divided into four groups: 1) prenatal stress + duloxetine treatment, 2) prenatal stress + vehicle, 3) duloxetine treatment alone, and 4) vehicle alone. Adult offspring were assessed for anxiety-like behavior using the open field test and depression-like behavior using the forced swim test. Brains were analyzed for pro-inflammatory cytokine markers in the hippocampus via real-time PCR. Results demonstrate that prenatal stress-induced anxiety- and depression-like behaviors are associated with an increase in hippocampal inflammatory mediators, and duloxetine administration prevents the increased hippocampal pro-inflammatory cytokine interleukin-6 and anxiety- and depression-like behavior in prenatally stressed adult offspring. This research provides important evidence on the long-term effect of PNS exposure during development in a model of maternal adversity to study the pathogenesis of depression and its therapeutic interventions.     

Maternal administration of magnesium sulfate promotes cell proliferation in hippocampus dentate gyrus in offspring mice after exposing to prenatal stress

Prenatal stress (PS) inhibits cell proliferation in the hippocampal dentate gyrus (DG), which is related to hippocampal anatomy and function abnormality. The aim of the study was to investigate the effects of magnesium sulfate (MgSO₄) on PS-induced cell proliferation suppression in offspring during embryonic stage and postnatal spatial learning. MgSO₄ administration was performed after PS treatment on pregnant mice. Mice were randomly divided into four groups: non-PS or PS maternal mice injected with MgSO₄ or saline (P + NS, P + MG, C + MG and C + NS group). Corticosterone was collected from amniotic fluid of mother mice on day 17 of embryonic stage (E17). The ability for spatial learning and memory of pups postnatal 3 week was evaluated using water maze assay. Additionally, cell proliferation was detected by assessing the expression of Ki67 using immunohistochemistry in mice fetuses or pups. PS significantly increased corticosterone level in amniotic fluid (P < 0.05) and impaired the spatial learning and memory (P + NS vs C + NS of latency time and track path length: P < 0.05) of offspring on postnatal day 21. However, MgSO₄ administration could reverse PS-induced spatial learning and memory disability (P + MG vs P + NS, P < 0.05). Additionally, PS reduced the number of Ki67-positive cell in hippocampal DG on E17, E19 and postnatal day 21 (P + NS vs C + NS, P < 0.05), which were also abrogated by maternal administration of MgSO₄ (P + MG vs P + NS, P < 0.05). Collectively, prenatal administration of MgSO₄ can reverse PS-induced reduction of cell proliferation in hippocampal DG during embryonic stage and postnatal spatial learning.     

Behavior ontogeny in the elevated plus-maze: prenatal stress effects

Prenatal stress is a putative model for studying some psychopathological disorders. Indeed, submitting pregnant animals to stress leads to enhanced anxiety in the adult offspring. However, little is known about how prenatal stress effects interacts with anxiety throughout development. To study this issue, prenatally stressed rats were tested in the elevated plus-maze at different ages. During pregnancy female rats were submitted to uncontrollable electric foot shock sessions every other day or kept undisturbed (controls). After delivery, litters from control and stressed dams were left undisturbed from the 3rd to the 14th postnatal days. Male and female rats were tested in the elevated plus-maze at the ages of 30, 45 or 60 days. The following measures were taken in the elevated plus-maze: number of entries and time spent in the arms (or their extremities) and frequency and time spent in naturalistic behaviors (stretching, rearing, end exploring, grooming and head dipping). Decreases in the percentage of entries into and in the time spent (only females) in the open arms were shown by 60-day-old prenatally stressed rats, but not by 30- and 45-day old. Increased open arm ends exploration was shown by 45-day-old prenatally stressed males. Rearing behavior was found to increase with age, a phenomenon more pronounced in females. Additionally, at the younger ages prenatally stressed rats were heavier than controls, an effect which disappeared at young adulthood. In conclusion, anxiogenic prenatal stress effects in the elevated plus-maze could only be detected at early adulthood, not before. Nonetheless, at late adolescence (45 days of age) prenatal stress leaded to an anxiolytic-like effect which can be interpreted as increased risk-taking behavior.     

Strain-dependent effects of prenatal maternal immune activation on anxiety- and depression-like behaviors in offspring

There is converging evidence that prenatal maternal infection can increase the risk of occurrence of neuropsychiatric disorders like schizophrenia, autism, anxiety and depression in later life. Experimental studies have shown conflicting effects of prenatal maternal immune activation on anxiety-like behavior and hypothalamic–pituitary–adrenal (HPA) axis development in offspring. We investigated the effects of maternal immune activation during pregnancy on anxiety- and depression-like behaviors in pregnant mice and their offspring to determine whether these effects are dependent on strain. NMRI and C57BL/6 pregnant mice were treated with either saline or lipopolysaccharide on gestational day 17 and then interleukin (IL)-6 and corticosterone (COR) levels; anxiety or depression in the pregnant mice and their offspring were evaluated. The results indicate that maternal inflammation increased the levels of COR and anxiety-like behavior in NMRI pregnant mice, but not in C57BL/6 dams. Our data also demonstrate that maternal inflammation elevated the levels of anxiety-and depression-like behaviors in NMRI offspring on the elevated plus-maze, elevated zero-maze, tail suspension test and forced swimming test respectively, but not in the open field and light–dark box. In addition, we did not find any significant change in anxiety- and depression-like behaviors of adult C57BL/6 offspring. Our findings suggest that prenatal maternal immune activation can alter the HPA axis activity, anxiety- and depression-like behaviors in a strain- and task-dependent manner in offspring and further comprehensive studies are needed to prove the causal relationship between the findings found here and to validate their relevance to neuropsychiatric disorders in humans.