Down-regulation of BDNF mRNA, with no effect on trkB or glucocorticoid receptor m RNAs, in the porcine hippocampus after acute dexamethasone treatment

Glucocorticoids bind to hippocampal mineralo-(MR) and gluco-(GR) corticoid receptors and, at high concentrations (e.g. as seen following treatment with pharmacological doses of corticosteroids or during stress), may affect hippocampal neuronal function. Such actions could involve brain-derived neurotrophic factor (BDNF), its receptor, trkB, and the excitatory neurotransmitter, glutamate. This experiment investigated the effect of a single intravenous (i.v.) injection of the synthetic glucocorticoid, dexamethasone (Dex, 5 mg kg(-1)) on gene expression for MR s, GR s, BDNF, trkB, and selected ionotropic glutamate receptor subunits (iGluRs), in the porcine hippocampus. Quantification of m RNA s in the brains of pigs (n = 4/treatment) killed 24 hours after saline or Dex administration indicated a significant Dex-induced decrease in BDNF m RNA in all hippocampal regions. However, gene expression for MR s, GR s, trkB and iGluRs was unaffected at this time-point.     

牦牛CRH基因克隆及其在生殖轴中的表达研究

为了探讨促肾上腺皮质激素释放激素（corticotropin-releasing hormone，CRH）基因在牦牛繁殖中的调控作用，试验分别采集5头成年母牦牛和5头成年母黄牛的下丘脑、脑垂体前叶、输卵管、卵巢和子宫等组织，通过RT-PCR技术及生物信息学软件对牦牛CRH基因编码区进行扩增、克隆及序列分析，并构建系统进化树；采用实时荧光定量PCR法检测CRH基因的组织表达。结果表明，牦牛CRH基因编码区全长573 bp，编码190个氨基酸。牦牛与黄牛、猫、鸡、人、小鼠、大鼠和猪的CRH基因核苷酸同源性分别为99.8%、43.3%、36.1%、46.2%、39.0%、38.5%和56.4%。系统进化树表明，牦牛与黄牛亲缘关系最近，并与其他物种类聚，符合物种进化规律。CRH蛋白分子式为C₉₂₀H₁₅₀₃N₂₇₉O₂₆₃S₃，分子质量为20776.95 u，理论等电点为10.95，其氨基酸组成中亮氨酸（L）、脯氨酸（P）、丙氨酸（A）和精氨酸（R）所占比例较高，分别为15.8%、12.6%、12.1%和10.5%。CRH蛋白为不稳定亲水蛋白，存在信号肽和跨膜结构。CRH蛋白二级结构中α-螺旋、β-转角、延伸链和无规则卷曲分别占41.05%、1.05%、8.42%和49.48%，三级结构分析结果与其相一致。CRH基因mRNA在牦牛下丘脑中表达量最高，显著高于其他组织（P<0.05），在子宫中表达量最低。牦牛脑垂体前叶CRH基因mRNA表达量极显著高于黄牛（P<0.01），在卵巢、输卵管中表达量显著高于黄牛（P<0.05），而两个品种在下丘脑、子宫中的表达量差异不显著（P>0.05）。提示CRH基因在牦牛繁殖调控中具有重要作用。     

The immediate effects of weaning stress on the hypothalamus‐pituitary‐adrenal alteration of newly weaned piglets

This study was conducted to examine the effects of weaning stress on gene expression of specific markers in hypothalamus‐pituitary‐adrenal (HPA) axis and neuronal activity in the newly weaned piglets. Twelve 28‐days‐old, newly weaned crossbred (Landrace × Yorkshire × Duroc) male piglets from 6 l (2 piglets/l) were randomly categorized into two groups: (a) weaning stress: piglets were separated from their dams, relocated and mixed with the unacquainted domestic piglets for 2 hr (stress, n = 6); (b) no‐stress: piglets stayed with their dams in the farrowing house (NS; n = 6). After weaning stress, all piglets were electrically euthanized and the blood samples/HPA tissues were collected for subsequent analysis, including plasma cortisol and mRNA expression of c‐fos, c‐jun, corticotropin‐releasing hormone (CRH), CRH receptor 1 (CRHR‐1) and adrenocorticotropin hormone receptor (MC2R). Results: Weaning stress significantly (p < 0.05) increased the plasma cortisol level and suppressed the expression of c‐fos and CRH in hypothalamus. In addition, weaning stress enhanced the mRNA abundance of c‐jun and CRHR‐1 in the pituitary gland. No significant differences in the gene expression of MC2R and CRHR‐1 were observed in the adrenal gland between treatment groups. Taken together, HPA involved in weaning stress and CRHR‐1 and c‐jun could be potential markers to evaluate the activation of HPA axis.     

Sequential alterations of glucocorticoid receptors in the hippocampus of STZ-treated type 1 diabetic rats

Type 1 diabetes is a common metabolic disorder accompanied by increased blood glucose levels along with glucocorticoid and cognitive deficits. The disease is also thought to be associated with environmental changes in brain and constantly induces oxidative stress in patients. Therefore, glucocorticoid-mediated negative feedback mechanisms involving the glucocorticoid receptor (GR) binding site are very important to understand the development of this disease. Many researchers have used streptozotocin (STZ)-treated diabetic animals to study changes in GR expression in the brain. However, few scientists have evaluated the hyperglycemic period following STZ exposure. In the present study, we found GR expression in the hippocampus varied based on the period after STZ administration for up to 4 weeks. We performed immunohistochemistry and Western blotting to validate the sequential alterations of GR expression in the hippocampus of STZ-treated type 1 diabetic rats. GR protein expression increased significantly until week 3 but decreased at week 4 following STZ administration. GR expression after 70 mg/kg STZ administration was highest at 3 weeks post-treatment and decreased thereafter. Although STZ-induced increase in GR expression in diabetic animals has been described, our data indicate that researchers should consider the sequential GR expression changes during the hyperglycemic period following STZ exposure.     

In vitro and in vivo temporal aspects of ACTH secretion: stimulatory actions of corticotropin-releasing hormone and vasopressin in cattle

The objective of the present study was to evaluate the temporal aspects associated with corticotropin-releasing hormone (CRH) and vasopressin (VP) stimulated bovine adrenocorticotropic hormone (ACTH) secretion in vitro and in vivo. For the in vitro studies, bovine anterior pituitary glands were enzymatically dispersed to establish primary cultures. On day 5 of culture, cells were challenged for 3 h with medium alone (Control) or various combinations and concentrations of bovine CRH (bCRH) and VP. Both CRH and VP each increased (P < 0.05) ACTH secretion. Maximal increases in ACTH secretion occurred in response to 0.1 microM CRH (5.5-fold) and 1 microM VP (3.7-fold), relative to Control cells. The in vivo portion of the study examined possible temporal differences in the activation of the pituitary-adrenal axis by CRH and VP. Jersey cows were randomly assigned to one of four groups (n = 8 cows/group): (i) Control (saline); (ii) bCRH (0.3 microg/kg BW); (iii) VP (1 microg/kg BW) and (iv) bCRH (0.3 microg/kg BW) + VP (1 microg/kg BW). Jugular blood samples were collected at 15-min intervals for 4 h pre- and for 6 h post-treatment; samples were also taken at 1, 5 and 10 min post-treatment. Plasma concentration of ACTH did not differ among treatment groups for the 4-h pre-treatment period. At 1 min post-treatment, bCRH + VP, VP and bCRH increased ACTH secretion by 22.4-, 9.6- and 2.2-fold, respectively, relative to Control (32.7 +/- 7.2 pg/ml). Maximal plasma concentration of ACTH occurred at 5, 10 and 15 min post-treatment for the VP (1017.7 +/- 219.9 pg/ml), bCRH + VP (1399.8 +/- 260.1 pg/ml) and bCRH (324.8 +/- 126.2 pg/ml) treatment groups respectively. Both the in vitro and in vivo data demonstrated that while VP acutely activates the bovine pituitary-adrenal axis, CRH-induced ACTH secretion is slower in onset but of longer duration. The present study also provides insight into the dynamics of ACTH and cortisol (CS) responsiveness to CRH and VP in cattle.     

Regulation of CRF, POMC and MC4R gene expression after electrical foot shock stress in the rat amygdala and hypothalamus

We investigated the effects of electrical foot shock stress on the melanocortin signaling cascade and the hypothalamus-pituitary-adrenal (HPA) system by observing levels of mRNA expression of corticotropin releasing factor (CRF), pro-opiomelanocortin (POMC), and melanocortin receptor subtype 4 (MC4R) in the rat amygdala and hypothalamus. When rats were exposed to electrical shock for 0.5 hr or 1 hr, plasma ACTH and corticosterone concentrations increased, indicating stress. The rats were then sacrificed to obtain RNA preparations from the brain tissue. In the amygdala, the expression of MC4R and POMC mRNA as well as CRF mRNA was significantly increased by electrical foot shock stress. In the hypothalamus, MC4R and POMC mRNA increased, but CRF mRNA remained unchanged. The duration of increased gene expression of MC4R and POMC in the amygdala was more sustained than in the hypothalamus. These results have provided the first evidence that exposure to stress increases expression of the MC4R system in the amygdala and hypothalamus.     

下丘脑-垂体-肾上腺轴参与动物采食调控的研究进展

采食是动物维持生命活动的基本生理过程，是动物生长发育的基础。畜禽采食量的高低直接影响到营养物质的摄入量及生产性能的发挥。在畜牧业生产中，影响采食的因素很多，而应激是其中一个非常重要的影响因素。动物机体的应激反应主要由下丘脑-垂体-肾上腺（HPA）轴来调控。下丘脑、垂体和肾上腺皮质通过释放促肾上腺皮质激素释放激素（CRH）、促肾上腺皮质激素（ACTH）和糖皮质激素（GC）这3种应激激素来协同调控动物的应激反应。应激激素对采食行为的调节是一个非常复杂的过程，主要通过稳态和非稳态途径来调节采食，可以双向调控食物的摄入量。稳态途径指的是通过调控机体能量稳态而调控采食。CRH和ACTH通过抑制下丘脑促食欲肽的表达而抑制采食；而GC在中枢和外周发挥着完全相反的作用。非稳态途径指的是通过影响中脑奖赏系统调控采食的愉悦感，是近年来食欲调控研究的热点，越来越多的研究证明了应激激素与奖赏系统的联系。作者针对应激激素调控采食的最新研究报道进行综述，以期为生产实践中新型的采食调控技术研发提供一定的参考。     

新Ⅰ型鸭肝炎病毒VP1和3D蛋白的原核表达及鉴定

为表达新Ⅰ型亚肝炎病毒(DHV-1C)的VP1和3D重组蛋白,本研究根据GenBank中的DHV-1C N株全基因序列,设计合成两对引物扩增其VP1和3D基因,构建重组表达载体并进行诱导表达.SDS-PAGE和western blot分析表明,VP1和3D重组蛋白分别在诱导3h和4h后表达量达到峰值,其大小分别为37.68 ku和65.80 ku,并且能够与抗DHV-1C阳性血清产生特异性免疫反应.     

鹅细小病毒VP3基因真核表达载体的构建及其在Vero细胞中表达

根据已发表的鹅细小病毒(GPV)B株核苷酸序列,设计并合成了1对引物,PCR扩增GPV吉林分离株主要结构蛋白VP3基因,获得大小为1605bp的核苷酸片段。将该片段纯化后克隆入pMD18-T载体,转化感受态大肠杆菌JM109,双酶切鉴定,筛选阳性重组质粒并测序。经过酶切和连接反应,将VP3基因克隆入真核表达载体pVAX1,转化感受态大肠杆菌DH5α,筛选阳性克隆,提取质粒,进行了PCR和酶切鉴定。通过脂质体法将pVAX1-VP3转染Vero细胞,RT-PCR和间接免疫荧光法检测。结果显示,VP3基因克隆成功,与GPVB株核苷酸序列同源性为96.2%;PCR和酶切鉴定结果证实,成功构建了含VP3基因的GPV真核表达载体pVAX1-VP3。提取转染该质粒的Vero细胞RNA,RT-PCR扩增,在1000～2000bp可见一明显DNA条带;间接荧光抗体染色转染细胞,在细胞表面可见特异荧光。     

制动应激对孕猪海马结构神经元可塑性的影响

旨在研究限位栏饲养造成的制动应激对妊娠母猪神经元可塑性的影响，本研究选取6头8~9月龄配种成功的巴马小型母猪，随机分成两组，应激组（n=3）限位栏饲养，对照组（n=3）自由环境饲养，其余饲养管理一致。于妊娠第18天处死孕猪，取其海马和血液，使用ELISA、放射免疫法检测相关激素水平，制作海马石蜡切片进行尼氏染色和镀银染色后观察神经元丢失率、树突复杂度以及树突棘数量等，并采用Western blot检测海马脑源性神经营养因子（BDNF）表达水平。结果显示，应激组血浆中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（COR）水平均显著上升（P≤0.05），齿状回（DG）和CA3区出现神经元丢失现象，CA3区锥形细胞树突复杂度下降，神经元成熟树突棘和未成熟树突棘数量均显著降低，DG的成熟树突棘数量显著降低，且海马内的BDNF蛋白表达量较对照组降低70.6%（P≤0.01）。因此，制动应激减弱了孕猪大脑海马中CA3区和DG的神经元可塑性。     

Effect of dexamethasone on hypothalamic expression of appetite-related genes in chickens under different diet and feeding conditions

Background: Glucocorticoids(GCs) are involved in the control of appetite in birds and mammals. The effect of GCs on feed intake in birds depends on their dietary energy level. But the regulation mechanism of GCs on appetite is still unclear in chickens facing to different energy level. An experiment was conducted to investigate the effect of dexamethasone(DEX) on hypothalamic expression of appetite-related peptides in chickens fed high/low fat diet and under fasting/feeding condition.Results: An interaction between DEX injection and dietary energy level was found on hypothalamic corticotropinreleasing hormone(CRH) gene expression in fasted chickens(P 0.05). The chickens, given a DEX injection and a low fat diet treatment, had the highest CRH m RNA levels than any of the fasted chickens given treatments(P 0.05).Under fasting conditions, the DEX treatment significantly increased hypothalamic neuropeptide Y(NPY) and GC receptors m RNA levels(P 0.05). Under re-feeding conditions, DEX treatment significantly decreased hypothalamic expression levels of NPY and agouti-related peptide(Ag RP) but significantly increased the level of hypothalamic CRH expression(P 0.05).Conclusion: A regulatory network formed by NPY, Ag RP and CRH is associated with the appetite-control by GCs.The result suggests that the regulation of GCs on orexigenic neuropeptides expression is dependent at least partially on dietary energy level and feeding state.     

The enhanced expression of c-Jun immunoreactivity in the adrenalectomized gerbil hippocampus

Recent in vitro and in vivo studies have shown that glucocorticoids have a profound influence on the survival of hippocampal neurones, and that the depletion of glucocorticoids as a result of adrenalectomy (ADX) reduces nerve growth factor levels in the hippocampus. It is also believed that ADX is associated with the seizure susceptibility of the Mongolian gerbil. In the present study, the choronological changes of c-jun immunoreactivity were investigated after ADX in the hippocampal formations in the seizure-prone gerbil model. In the sham hippocampus, c-jun immunoreactivity was not observed in the neurones of the hippocampus proper and dentate gyrus. C-jun immunoreactive neurones appeared 3 h after ADX in the neurones of the CA1 area and dentate gyrus, and these immunoreactivities peaked 24 h after ADX and then gradually decreased. These results suggest that, in the adrenalectomized gerbil, c-jun may be expressed in the neurones of the hippocampus in compensation for glucocorticoid deficit. The result of enhanced c-jun expression of the hippocampal formation provides anatomical support for the hypothesis that c-jun may play a role in the reduction of seizure activity.     

Involvement of granulin in estrogen-induced neurogenesis in the adult rat hippocampus

Recent studies have demonstrated the presence of neurogenesis in the adult mammalian hippocampus, and it has been suggested that estrogen and various growth factors influence the processes of adult neurogenesis. The present study assessed cell proliferation in the dentate gyrus and the mRNA expression levels of granulin, insulin-like growth factor-I (IGF-I), and brain-derived neurotrophic factor (BDNF) in the hippocampus 4 h after treatment with estradiol benzoate (EB) in 3- and 12-month old ovariectomized rats. At 3 months of age, mRNA expression of granulin precursor and cell proliferation were increased by EB treatment, although the mRNA expressions of IGF-I and BDNF remained unchanged. At 12 months of age, however, neither mRNA expression of the three genes nor cell proliferation in the dentate gyrus were affected by EB treatment. In addition, 17beta-estradiol enhanced the proliferation of neural progenitor cells derived from hippocampal tissue of 3-month-old female rats in vitro; this was inhibited by neutralization of granulin with specific antibody. These results suggest that estrogen induces granulin gene expression in the hippocampus and that the product of this gene is involved in the mitogenic effects of estrogen in the dentate gyrus, although the responses to estrogen decline with age.     

Effects of dizocilpine pretreatment on parvalbumin immunoreactivity and Fos expression after cerebral ischemia in the hippocampus of the Mongolian gerbil

The mechanisms of ischemic neuronal death have been focused on glutamate receptor activation and subsequent elevation of intracellular Ca2+ concentration. The purpose of this study was to evaluate the effects of dizocilpine, an NMDA receptor antagonist, pretreatment on Fos expression and parvalbumin (PV, calcium binding protein) immunoreactivity in the hippocampus of the mongolian gerbil after global ischemic insults. The number of PV-immunoreactive (PV-ir) neurons in CA1 were significantly decreased from 1 day after cerebral ischemia, while dizocilpine pretreatment completely suppressed the loss of PV-ir neurons in CA1. Dizocilpine pretreatment also protected the structural loss of microtubule-associated protein 2 immunoreactivity in CA1 after ischemic insults. In addition, dizocilpine pretreatment increased Fos expression in both hippocampal CA3 and CA4 after 3 hr ischemic reperfusion as compared to that of the saline pretreated group. Subsequently, the Fos-defined cellular activity of PV-ir neurons was slightly increased by dizocilpine pretreatment in the hippocampal area. This study demonstrated that NMDA receptor mediated calcium influx was associated with the loss of PV-ir neurons in CA1 hippocampal region, and that dizocilpine pretreatment increased Fos expression and the neuronal activity of PV-ir neurons in the non-vulnerable region of hippocampus after cerebral ischemia. Based on this data, we conclude that the protective effect of dizocilpine may be induced by the regulation of calcium overload, or by the upregulation of a neuroregenerative initiator such as Fos protein.     

Evaluation of exogenous glucocorticoid injection on preweaning growth performance of neonatal pigs under commercial conditions

Three commercial trials were conducted to evaluate the use of dexamethasone (Dex) and/ or isoflupredone (Predef) in improving preweaning growth performance of neonatal pigs. The objectives of the commercial trials were threefold: 1) to evaluate Predef in comparison with Dex; 2) to address the sexual dimorphic growth response observed in a previous commercial trial; and 3) to determine whether there is any benefit of providing Dex treatment to pigs being fed supplemental milk. In Exp. 1, 276 pigs (Triumph 4 x PIC Camborough 22) were assigned according to birth weight and sex to three treatments. Treatments included saline (Control), Dex (2 mg/kg BW i.m. injection of Dex), or Predef (2 mg/kg BW i.m. injection of Predef 2X) within 24 h after birth. A treatment effect was observed for BW at weaning (P < 0.001), with pigs injected with Predef being 0.51 kg lighter than Control and Dex-treated pigs. The lower BW of Predef-treated pigs at weaning were a result of a lower ADG (P < 0.001) during the preweaning period compared with Control and Dex pigs. In Exp. 2, 703 pigs (Triumph 4 x PIC Camborough 22) were assigned according to birth weight and sex to three treatments. Treatments included either an i.m. injection of saline (Control), Dexl (1 mg/kg BW of Dex), or Dex2 (2 mg/kg BW of Dex) within 24 h after birth. No treatment effects were observed for BW at weaning (P = 0.24) or ADG (P = 0.19). In Exp. 3, 342 pigs (Genetiporc) were assigned according to birth weight and sex to two treatments. Treatments included either an i.m. injection of saline or Dex (2 mg/kg BW) within 24 h after birth. All pigs were provided supplemental milk from the time of treatment until weaning age. No treatment effects were observed for BW at weaning (P = 0.13) or ADG (P = 0.11). The negative response to Predef was similar to the growth-suppressive effects observed by others using chronic glucocorticoid treatment. In contrast to our previous findings, Dex did not improve preweaning growth performance regardless of dose or supplemental milk.     

Maternal social stress during late pregnancy affects hypothalamic-pituitary-adrenal function and brain neurotransmitter systems in pig offspring

Maternal stress in pregnant sows may induce long-lasting alterations in the behavior, physiology, and immunity of their offspring. The aim of the present study was to investigate the consequences of repeated social stress during late gestation on determinants of the hypothalamic–pituitary–adrenal axis and on hippocampal neurotransmitter profiles in pig offspring. All pregnant gilts were housed in pairs. Each Stress gilt was mixed with an unfamiliar gilt twice a week between days 77 and 105 of gestation (n = 18). Control gilts were housed in stable pairs over the same period (n = 18). Plasma cortisol and corticosteroid binding globulin (CBG) were measured in 1 male and 1 female per litter in a basal situation on postnatal days (PND) 4, 26, and 60 and in a stressful situation at PND 28 (2 d after weaning) and 62 (2 d after relocation to a new building). Prenatal stress had no effect on plasma cortisol, but it decreased CBG at PND 26. Brain and adrenals were collected from 1 female per litter after weaning or relocation at PND 28 and PND 62. Adrenals were additionally collected at PND 4. Glucocorticoid receptor binding in the hippocampus and hypothalamus was not affected by prenatal treatment. However, prenatal stress increased the expression of 11β-hydroxysteroid dehydrogenase type 1 mRNA in the hippocampus after weaning (P < 0.05) and after relocation (P = 0.08). In addition, prenatally stressed piglets showed an increased 5-hydroxyindole-3-acetic acid to 5-hydroxytryptamine ratio in the hippocampus after weaning and increased hippocampal c-fos mRNA expression and noradrenaline concentration after relocation (P < 0.05). Prenatal stress also increased the relative adrenal weight at PND 4 and the cell density in the cortex and the medulla at PND 28, whereas no difference was found for activities of catecholamine-synthesising enzymes in the medulla. Overall, our data indicate that repeated social stress during pregnancy has long-lasting consequences on hypothalamic–pituitary–adrenal axis and hippocampal neurotransmitter activity in the offspring of pigs.     

Temporal appearance of structural and nonstructural bluetongue viral proteins in infected cells, as determined by immunofluorescence staining and flow cytometry

The temporal appearance of 4 viral proteins was detected in bluetongue virus (BTV)-infected Vero cells by indirect immunofluorescence staining with monoclonal antibodies (MAb) to BTV structural proteins VP2 and VP7 and nonstructural proteins NS1 and NS2. Bluetongue viral proteins were detected at distinct intervals after inoculation of Vero cells; VP7 was first detected 3 hours after inoculation, NS1 and NS2 at 5 hours after inoculation, whereas VP2 was not detected until 8 hours after inoculation. Patterns of fluorescence varied with the fixative used, but each MAb induced a distinct pattern of fluorescence in infected cells. Flow cytometry, which was used with each of the 4 MAb, proved to be an accurate and sensitive method of detecting BTV-infected P3 mouse myeloma cells. The temporal appearance of each viral protein in BTV-infected P3 cells was similar to that detected in BTV-infected Vero cells. Advantages of flow cytometry over conventional immunofluorescence staining to detect BTV-infected cells included: (1) enumeration of the proportion of infected cells in a population; (2) further characterization of infected cells, including estimates of their viability; and (3) computer-assisted storage and analysis of data obtained.     

Corticosterone induced apoptosis of mouse oviduct epithelial cells independent of the TNF-α system

It has been reported in recent studies that restraint stress on pregnant mice during the preimplantation stage elevated corticotrophin-releasing hormone (CRH) and glucocorticoid levels in the serum and oviducts; furthermore, CRH and corticosterone (CORT) impacted preimplantation embryos indirectly by triggering the apoptosis of oviductal epithelial cells (OECs) through activation of the Fas system. However, it remains unclear whether TNF-α signaling is involved in CRH- and/or glucocorticoid-induced apoptosis of OECs. In the present study, it was shown that culture with either CRH or CORT induced significant apoptosis of OECs. The culture of OECs with CRH augmented both FasL expression and TNF-α expression. However, culture with CORT increased FasL, but decreased TNF-α, expression significantly. Although knocking down/knocking out FasL expression in OECs significantly ameliorated the proapoptotic effects of both CRH and CORT, knocking down/knocking out TNF-α expression relieved only the proapoptotic effect of CRH but not that of CORT. Taken together, our results demonstrated that CRH-induced OEC apoptosis involved both Fas signaling and TNF-α signaling. Conversely, CORT-induced OEC apoptosis involved only the Fas, but not the TNF-α, signaling pathway. The data obtained are crucial for our understanding of the mechanisms by which various categories of stress imposed on pregnant females impair embryo development, as well as for the development of measures to protect the embryo from the adverse effects of stress.