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Stephen G Matthews - One of the best experts on this subject based on the ideXlab platform.
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Prenatal Stress modifies behavior and hypothalamic pituitary adrenal function in female guinea pig offspring effects of timing of Prenatal Stress and stage of reproductive cycle
Endocrinology, 2008Co-Authors: Amita Kapoor, Stephen G MatthewsAbstract:Prenatal Stress is associated with altered behavior and hypothalamic-pituitary-adrenal (HPA) axis function postnatally. Recent studies suggest that these outcomes are dependent on the timing of the Prenatal Stress. The majority of these studies have been carried out in male offspring. We hypothesized that a short period of Prenatal Stress would result in female offspring that exhibit differences in open-field behavior and HPA axis activity, but the outcome would depend on the timing of the Prenatal Stress and the stage of the reproductive cycle. Pregnant guinea pigs were exposed to a strobe light during the fetal brain growth spurt [gestational d 50-52 (PS50)] or during the period of rapid brain myelination [gestational d 60-62 (PS60)]. Open-field activity was assessed in juvenile and adult female offspring. HPA axis function was tested in adult offspring. All tests in adulthood were carried out during the estrous and luteal phases of the reproductive cycle to determine the effect of stage on HPA axis programming. Tissues were collected upon completion of the study for analysis by in situ hybridization. PS60 offspring exhibited decreased activity in an open field during the estrous phase of the reproductive cycle compared with control offspring. Both PS50 and PS60 offspring exhibited a lower salivary cortisol response to a Stressor, only during the estrous phase. Consistent with the behavioral and endocrine data, PS60 females exhibited lower plasma estradiol levels, reduced ovary weight, and increased glucocorticoid receptor mRNA in the paraventricular nucleus. In conclusion, we have demonstrated that there are effects of Prenatal Stress on behavior and HPA axis functioning in female offspring but that the outcomes are dependent on the timing of the Prenatal Stress together with the status of the reproductive cycle.
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fetal programming of hypothalamo pituitary adrenal function Prenatal Stress and glucocorticoids
The Journal of Physiology, 2006Co-Authors: Amita Kapoor, Elizabeth Dunn, Alice Kostaki, Marcus H Andrews, Stephen G MatthewsAbstract:Prenatal Stress (PS) and maternal exposure to exogenous glucocorticoids can lead to permanent modification of hypothalamo-pituitary-adrenal (HPA) function and Stress-related behaviour. Both of these manipulations lead to increased fetal exposure to glucocorticoids. Glucocorticoids are essential for many aspects of normal brain development, but exposure of the fetal brain to an excess of glucocorticoids can have life-long effects on neuroendocrine function. Both endogenous glucocorticoid and synthetic glucocorticoid exposure have a number of rapid effects in the fetal brain, including modification of neurotransmitter systems and transcriptional machinery. Such fetal exposure permanently alters HPA function in prepubertal, postpubertal and ageing offspring, in a sex-dependent manner. Prenatal Stress and exogenous glucocorticoid manipulation also lead to the modification of behaviour, brain and organ morphology, as well as altered regulation of other endocrine systems. It is also becoming increasingly apparent that the timing of exposure to PS or synthetic glucocorticoids has tremendous effects on the nature of the phenotypic outcome. Permanent changes in endocrine function will ultimately impact on health in both human and animal populations.
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short periods of Prenatal Stress affect growth behaviour and hypothalamo pituitary adrenal axis activity in male guinea pig offspring
The Journal of Physiology, 2005Co-Authors: Amita Kapoor, Stephen G MatthewsAbstract:Prenatal Stress can have profound long-term influences on physiological function throughout the course of life. We hypothesized that focused periods of moderate Prenatal Stress at discrete time points in late gestation have differential effects on hypothalamo–pituitary–adrenal (HPA) axis function in adult guinea pig offspring, and that changes in HPA axis function will be associated with modification of anxiety-related behaviour. Pregnant guinea pigs were exposed to a strobe light for 2 h on gestational days (GD) 50, 51, 52 (PS50) or 60, 61, 62 (PS60) (gestation length ∼70 days). A control group was left undisturbed throughout pregnancy. Behaviour was assessed in male offspring on postnatal day (PND)25 and PND70 by measurement of ambulatory activity and thigmotaxis (wall-seeking behaviour) in a novel open field environment. Subsequent to behavioural testing, male offspring were cannulated (PND75) to evaluate basal and activated HPA axis function. Body weight was significantly decreased in adult PS50 and PS60 offspring and this effect was apparent soon after weaning. The brain-to-body-weight ratio was significantly increased in adult PS50 males. Basal plasma cortisol levels were elevated in PS50 male offspring throughout the 24 h sampling period compared with controls. In response to an ACTH challenge and to exposure to an acute Stressor, PS60 male offspring exhibited elevated plasma cortisol responses. Plasma testosterone concentrations were strikingly decreased in PS50 offspring. Thigmotaxis in the novel environment was increased in PS50 male offspring at PND25 and PND70, suggesting increased anxiety in these animals. In conclusion, Prenatal Stress during critical windows of neuroendocrine development programs growth, HPA axis function, and Stress-related behaviour in adult male guinea pig offspring. Further, the nature of the effect is dependant on the timing of the maternal Stress during pregnancy.
Jodi L Pawluski - One of the best experts on this subject based on the ideXlab platform.
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developmental fluoxetine and Prenatal Stress effects on serotonin dopamine and synaptophysin density in the pfc and hippocampus of offspring at weaning
Developmental Psychobiology, 2016Co-Authors: Mary Gemmel, Christina Dalla, Ine Rayen, Tiffany Lotus, Eva L Van Donkelaar, Harry W M Steinbusch, Sonsoles De Lacalle, Nikolaos Kokras, Jodi L PawluskiAbstract:Selective serotonin reuptake inhibitor medication exposure during the perinatal period can have a long term impact in adult offspring on neuroplasticity and the serotonergic system, but the impact of these medications during early development is poorly understood. The aim of this study was to determine the effects of developmental exposure to the SSRI, fluoxetine, on the serotonergic system, dopaminergic system, and synaptophysin density in the prefrontal cortex and hippocampus, as well as number of immature neurons in the dentate gyrus, in juvenile rat offspring at weaning. To model aspects of maternal depression, Prenatal restraint Stress was used. Sprague-Dawley rat offspring were exposed to either Prenatal Stress and/or fluoxetine. Main findings show that developmental fluoxetine exposure to Prenatally Stressed offspring decreased 5-HT and 5-HIAA levels and altered the dopaminergic system in the hippocampus. Prenatal Stress, regardless of fluoxetine, increased synaptophysin density in the PFC. This work indicates that early exposure to maternal Stress and SSRI medication can alter brain monoamine levels and synaptophysin density in offspring at weaning.
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Developmental fluoxetine and Prenatal Stress effects on serotonin, dopamine, and synaptophysin density in the PFC and hippocampus of offspring at weaning
Developmental Psychobiology, 2016Co-Authors: Mary Gemmel, Christina Dalla, Ine Rayen, Tiffany Lotus, Harry W M Steinbusch, Sonsoles De Lacalle, Nikolaos Kokras, Eva Donkelaar, Jodi L PawluskiAbstract:Selective serotonin reuptake inhibitor medication exposure during the perinatal period can have a long term impact in adult offspring on neuroplasticity and the serotonergic system, but the impact of these medications during early development is poorly understood. The aim of this study was to determine the effects of developmental exposure to the SSRI, fluoxetine, on the serotonergic system, dopaminergic system, and synaptophysin density in the prefrontal cortex and hippocampus, as well as number of immature neurons in the dentate gyrus, in juvenile rat offspring at weaning. To model aspects of maternal depression, Prenatal restraint Stress was used. Sprague-Dawley rat offspring were exposed to either Prenatal Stress and/or fluoxetine. Main findings show that developmental fluoxetine exposure to Prenatally Stressed offspring decreased 5-HT and 5-HIAA levels and altered the dopaminergic system in the hippocampus. Prenatal Stress, regardless of fluoxetine, increased synaptophysin density in the PFC. This work indicates that early exposure to maternal Stress and SSRI medication can alter brain monoamine levels and synaptophysin density in offspring at weaning. © 2015 Wiley Periodicals, Inc. Dev Psychobiol
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developmental fluoxetine exposure and Prenatal Stress alter sexual differentiation of the brain and reproductive behavior in male rat offspring
Psychoneuroendocrinology, 2013Co-Authors: Ine Rayen, Harry W M Steinbusch, Jodi L Pawluski, Thierry CharlierAbstract:Summary Depression during pregnancy and postpartum is a significant health problem and affects up to 20% of women. While selective serotonin reuptake inhibitor (SSRI) medications are the drug of choice for treatment of maternal depression, the combined effect of maternal depression and perinatal SSRI exposure on offspring development is poorly investigated. Our aim was to determine the role of exposure to fluoxetine during development on sexual behavior and sexually dimorphic brain structures in male offspring using a rodent model of maternal adversity. Sprague-Dawley rat dams were Stressed during gestation and were chronically treated throughout lactation with either fluoxetine or vehicle beginning on postnatal day 1. Four groups of offspring were used: (1) Control + Vehicle, (2) Control + Fluoxetine, (3) Prenatal Stress + Vehicle, and (4) Prenatal Stress + Fluoxetine. We show here that developmental fluoxetine treatment decreases the anogenital distance in juvenile male offspring. In adult male offspring, maternal fluoxetine treatment results in a decrease in the number of intromissions, a longer latency to the first intromission, and a longer latency to the first ejaculation. Furthermore, developmental fluoxetine and/or Prenatal Stress decrease the area of the sexually dimorphic nucleus of the preoptic area (SDN-POA). Prenatal Stress, but not exposure to developmental fluoxetine, decreases the number of tyrosine hydroxylase (TH)-positive cells in anteroventral periventricular nucleus (AVPv) and the volume of the posterior bed nucleus of the stria terminalis (pBST) in male offspring. These results provide important evidence for the long-term impact of maternal adversity and maternal fluoxetine use on the development of primary endocrinology systems in juvenile and adult male offspring.
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fluoxetine during development reverses the effects of Prenatal Stress on depressive like behavior and hippocampal neurogenesis in adolescence
PLOS ONE, 2011Co-Authors: Ine Rayen, Harry W M Steinbusch, Jos Prickaerts, Daniel L A Van Den Hove, Jodi L PawluskiAbstract:Depression during pregnancy and the postpartum period is a growing health problem, which affects up to 20% of women. Currently, selective serotonin reuptake inhibitor (SSRIs) medications are commonly used for treatment of maternal depression. Unfortunately, there is very little research on the long-term effect of maternal depression and perinatal SSRI exposure on offspring development. Therefore, the aim of this study was to determine the role of exposure to fluoxetine during development on affective-like behaviors and hippocampal neurogenesis in adolescent offspring in a rodent model of maternal depression. To do this, gestationally Stressed and non-Stressed Sprague-Dawley rat dams were treated with either fluoxetine (5 mg/kg/day) or vehicle beginning on postnatal day 1 (P1). Adolescent male and female offspring were divided into 4 groups: 1) Prenatal Stress+fluoxetine exposure, 2) Prenatal Stress+vehicle, 3) fluoxetine exposure alone, and 4) vehicle alone. Adolescent offspring were assessed for anxiety-like behavior using the Open Field Test and depressive-like behavior using the Forced Swim Test. Brains were analyzed for endogenous markers of hippocampal neurogenesis via immunohistochemistry. Results demonstrate that maternal fluoxetine exposure reverses the reduction in immobility evident in Prenatally Stressed adolescent offspring. In addition, maternal fluoxetine exposure reverses the decrease in hippocampal cell proliferation and neurogenesis in maternally Stressed adolescent offspring. This research provides important evidence on the long-term effect of fluoxetine exposure during development in a model of maternal adversity.
Amita Kapoor - One of the best experts on this subject based on the ideXlab platform.
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Prenatal Stress modifies behavior and hypothalamic pituitary adrenal function in female guinea pig offspring effects of timing of Prenatal Stress and stage of reproductive cycle
Endocrinology, 2008Co-Authors: Amita Kapoor, Stephen G MatthewsAbstract:Prenatal Stress is associated with altered behavior and hypothalamic-pituitary-adrenal (HPA) axis function postnatally. Recent studies suggest that these outcomes are dependent on the timing of the Prenatal Stress. The majority of these studies have been carried out in male offspring. We hypothesized that a short period of Prenatal Stress would result in female offspring that exhibit differences in open-field behavior and HPA axis activity, but the outcome would depend on the timing of the Prenatal Stress and the stage of the reproductive cycle. Pregnant guinea pigs were exposed to a strobe light during the fetal brain growth spurt [gestational d 50-52 (PS50)] or during the period of rapid brain myelination [gestational d 60-62 (PS60)]. Open-field activity was assessed in juvenile and adult female offspring. HPA axis function was tested in adult offspring. All tests in adulthood were carried out during the estrous and luteal phases of the reproductive cycle to determine the effect of stage on HPA axis programming. Tissues were collected upon completion of the study for analysis by in situ hybridization. PS60 offspring exhibited decreased activity in an open field during the estrous phase of the reproductive cycle compared with control offspring. Both PS50 and PS60 offspring exhibited a lower salivary cortisol response to a Stressor, only during the estrous phase. Consistent with the behavioral and endocrine data, PS60 females exhibited lower plasma estradiol levels, reduced ovary weight, and increased glucocorticoid receptor mRNA in the paraventricular nucleus. In conclusion, we have demonstrated that there are effects of Prenatal Stress on behavior and HPA axis functioning in female offspring but that the outcomes are dependent on the timing of the Prenatal Stress together with the status of the reproductive cycle.
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fetal programming of hypothalamo pituitary adrenal function Prenatal Stress and glucocorticoids
The Journal of Physiology, 2006Co-Authors: Amita Kapoor, Elizabeth Dunn, Alice Kostaki, Marcus H Andrews, Stephen G MatthewsAbstract:Prenatal Stress (PS) and maternal exposure to exogenous glucocorticoids can lead to permanent modification of hypothalamo-pituitary-adrenal (HPA) function and Stress-related behaviour. Both of these manipulations lead to increased fetal exposure to glucocorticoids. Glucocorticoids are essential for many aspects of normal brain development, but exposure of the fetal brain to an excess of glucocorticoids can have life-long effects on neuroendocrine function. Both endogenous glucocorticoid and synthetic glucocorticoid exposure have a number of rapid effects in the fetal brain, including modification of neurotransmitter systems and transcriptional machinery. Such fetal exposure permanently alters HPA function in prepubertal, postpubertal and ageing offspring, in a sex-dependent manner. Prenatal Stress and exogenous glucocorticoid manipulation also lead to the modification of behaviour, brain and organ morphology, as well as altered regulation of other endocrine systems. It is also becoming increasingly apparent that the timing of exposure to PS or synthetic glucocorticoids has tremendous effects on the nature of the phenotypic outcome. Permanent changes in endocrine function will ultimately impact on health in both human and animal populations.
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short periods of Prenatal Stress affect growth behaviour and hypothalamo pituitary adrenal axis activity in male guinea pig offspring
The Journal of Physiology, 2005Co-Authors: Amita Kapoor, Stephen G MatthewsAbstract:Prenatal Stress can have profound long-term influences on physiological function throughout the course of life. We hypothesized that focused periods of moderate Prenatal Stress at discrete time points in late gestation have differential effects on hypothalamo–pituitary–adrenal (HPA) axis function in adult guinea pig offspring, and that changes in HPA axis function will be associated with modification of anxiety-related behaviour. Pregnant guinea pigs were exposed to a strobe light for 2 h on gestational days (GD) 50, 51, 52 (PS50) or 60, 61, 62 (PS60) (gestation length ∼70 days). A control group was left undisturbed throughout pregnancy. Behaviour was assessed in male offspring on postnatal day (PND)25 and PND70 by measurement of ambulatory activity and thigmotaxis (wall-seeking behaviour) in a novel open field environment. Subsequent to behavioural testing, male offspring were cannulated (PND75) to evaluate basal and activated HPA axis function. Body weight was significantly decreased in adult PS50 and PS60 offspring and this effect was apparent soon after weaning. The brain-to-body-weight ratio was significantly increased in adult PS50 males. Basal plasma cortisol levels were elevated in PS50 male offspring throughout the 24 h sampling period compared with controls. In response to an ACTH challenge and to exposure to an acute Stressor, PS60 male offspring exhibited elevated plasma cortisol responses. Plasma testosterone concentrations were strikingly decreased in PS50 offspring. Thigmotaxis in the novel environment was increased in PS50 male offspring at PND25 and PND70, suggesting increased anxiety in these animals. In conclusion, Prenatal Stress during critical windows of neuroendocrine development programs growth, HPA axis function, and Stress-related behaviour in adult male guinea pig offspring. Further, the nature of the effect is dependant on the timing of the maternal Stress during pregnancy.
Harry W M Steinbusch - One of the best experts on this subject based on the ideXlab platform.
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developmental fluoxetine and Prenatal Stress effects on serotonin dopamine and synaptophysin density in the pfc and hippocampus of offspring at weaning
Developmental Psychobiology, 2016Co-Authors: Mary Gemmel, Christina Dalla, Ine Rayen, Tiffany Lotus, Eva L Van Donkelaar, Harry W M Steinbusch, Sonsoles De Lacalle, Nikolaos Kokras, Jodi L PawluskiAbstract:Selective serotonin reuptake inhibitor medication exposure during the perinatal period can have a long term impact in adult offspring on neuroplasticity and the serotonergic system, but the impact of these medications during early development is poorly understood. The aim of this study was to determine the effects of developmental exposure to the SSRI, fluoxetine, on the serotonergic system, dopaminergic system, and synaptophysin density in the prefrontal cortex and hippocampus, as well as number of immature neurons in the dentate gyrus, in juvenile rat offspring at weaning. To model aspects of maternal depression, Prenatal restraint Stress was used. Sprague-Dawley rat offspring were exposed to either Prenatal Stress and/or fluoxetine. Main findings show that developmental fluoxetine exposure to Prenatally Stressed offspring decreased 5-HT and 5-HIAA levels and altered the dopaminergic system in the hippocampus. Prenatal Stress, regardless of fluoxetine, increased synaptophysin density in the PFC. This work indicates that early exposure to maternal Stress and SSRI medication can alter brain monoamine levels and synaptophysin density in offspring at weaning.
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Developmental fluoxetine and Prenatal Stress effects on serotonin, dopamine, and synaptophysin density in the PFC and hippocampus of offspring at weaning
Developmental Psychobiology, 2016Co-Authors: Mary Gemmel, Christina Dalla, Ine Rayen, Tiffany Lotus, Harry W M Steinbusch, Sonsoles De Lacalle, Nikolaos Kokras, Eva Donkelaar, Jodi L PawluskiAbstract:Selective serotonin reuptake inhibitor medication exposure during the perinatal period can have a long term impact in adult offspring on neuroplasticity and the serotonergic system, but the impact of these medications during early development is poorly understood. The aim of this study was to determine the effects of developmental exposure to the SSRI, fluoxetine, on the serotonergic system, dopaminergic system, and synaptophysin density in the prefrontal cortex and hippocampus, as well as number of immature neurons in the dentate gyrus, in juvenile rat offspring at weaning. To model aspects of maternal depression, Prenatal restraint Stress was used. Sprague-Dawley rat offspring were exposed to either Prenatal Stress and/or fluoxetine. Main findings show that developmental fluoxetine exposure to Prenatally Stressed offspring decreased 5-HT and 5-HIAA levels and altered the dopaminergic system in the hippocampus. Prenatal Stress, regardless of fluoxetine, increased synaptophysin density in the PFC. This work indicates that early exposure to maternal Stress and SSRI medication can alter brain monoamine levels and synaptophysin density in offspring at weaning. © 2015 Wiley Periodicals, Inc. Dev Psychobiol
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developmental fluoxetine exposure and Prenatal Stress alter sexual differentiation of the brain and reproductive behavior in male rat offspring
Psychoneuroendocrinology, 2013Co-Authors: Ine Rayen, Harry W M Steinbusch, Jodi L Pawluski, Thierry CharlierAbstract:Summary Depression during pregnancy and postpartum is a significant health problem and affects up to 20% of women. While selective serotonin reuptake inhibitor (SSRI) medications are the drug of choice for treatment of maternal depression, the combined effect of maternal depression and perinatal SSRI exposure on offspring development is poorly investigated. Our aim was to determine the role of exposure to fluoxetine during development on sexual behavior and sexually dimorphic brain structures in male offspring using a rodent model of maternal adversity. Sprague-Dawley rat dams were Stressed during gestation and were chronically treated throughout lactation with either fluoxetine or vehicle beginning on postnatal day 1. Four groups of offspring were used: (1) Control + Vehicle, (2) Control + Fluoxetine, (3) Prenatal Stress + Vehicle, and (4) Prenatal Stress + Fluoxetine. We show here that developmental fluoxetine treatment decreases the anogenital distance in juvenile male offspring. In adult male offspring, maternal fluoxetine treatment results in a decrease in the number of intromissions, a longer latency to the first intromission, and a longer latency to the first ejaculation. Furthermore, developmental fluoxetine and/or Prenatal Stress decrease the area of the sexually dimorphic nucleus of the preoptic area (SDN-POA). Prenatal Stress, but not exposure to developmental fluoxetine, decreases the number of tyrosine hydroxylase (TH)-positive cells in anteroventral periventricular nucleus (AVPv) and the volume of the posterior bed nucleus of the stria terminalis (pBST) in male offspring. These results provide important evidence for the long-term impact of maternal adversity and maternal fluoxetine use on the development of primary endocrinology systems in juvenile and adult male offspring.
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fluoxetine during development reverses the effects of Prenatal Stress on depressive like behavior and hippocampal neurogenesis in adolescence
PLOS ONE, 2011Co-Authors: Ine Rayen, Harry W M Steinbusch, Jos Prickaerts, Daniel L A Van Den Hove, Jodi L PawluskiAbstract:Depression during pregnancy and the postpartum period is a growing health problem, which affects up to 20% of women. Currently, selective serotonin reuptake inhibitor (SSRIs) medications are commonly used for treatment of maternal depression. Unfortunately, there is very little research on the long-term effect of maternal depression and perinatal SSRI exposure on offspring development. Therefore, the aim of this study was to determine the role of exposure to fluoxetine during development on affective-like behaviors and hippocampal neurogenesis in adolescent offspring in a rodent model of maternal depression. To do this, gestationally Stressed and non-Stressed Sprague-Dawley rat dams were treated with either fluoxetine (5 mg/kg/day) or vehicle beginning on postnatal day 1 (P1). Adolescent male and female offspring were divided into 4 groups: 1) Prenatal Stress+fluoxetine exposure, 2) Prenatal Stress+vehicle, 3) fluoxetine exposure alone, and 4) vehicle alone. Adolescent offspring were assessed for anxiety-like behavior using the Open Field Test and depressive-like behavior using the Forced Swim Test. Brains were analyzed for endogenous markers of hippocampal neurogenesis via immunohistochemistry. Results demonstrate that maternal fluoxetine exposure reverses the reduction in immobility evident in Prenatally Stressed adolescent offspring. In addition, maternal fluoxetine exposure reverses the decrease in hippocampal cell proliferation and neurogenesis in maternally Stressed adolescent offspring. This research provides important evidence on the long-term effect of fluoxetine exposure during development in a model of maternal adversity.
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Prenatal Stress and neonatal rat brain development
Neuroscience, 2006Co-Authors: D L A Van Den Hove, Harry W M Steinbusch, Arjan Scheepens, W D J Van De Berg, L A M Kooiman, B J G Boosten, Jos Prickaerts, Carlos E BlancoAbstract:Chronic or repeated Stress during human fetal brain development has been associated with various learning, behavioral, and/or mood disorders, including depression in later life. The mechanisms accounting for these effects of Prenatal Stress are not fully understood. The aim of this study was to investigate the effects of Prenatal Stress on early postnatal brain development, a disturbance of which may contribute to this increased vulnerability to psychopathology. We studied the effects of Prenatal Stress on fetal growth, Stress-induced corticosterone secretion, brain cell proliferation, caspase-3-like activity and brain-derived neurotrophic factor protein content in newborn Fischer 344 rats. In addition to a slight reduction in birth weight, Prenatal Stress was associated with elevated corticosterone levels (33.8%) after 1 h of maternal deprivation on postnatal day 1, whereas by postnatal day 8 this pattern was reversed (-46.5%). Further, Prenatal Stress resulted in an approximately 50% decrease in brain cell proliferation just after birth in both genders with a concomitant increase in caspase-3-like activity within the hippocampus at postnatal day 1 (36.1%) and at postnatal day 5 (females only; 20.1%). Finally, brain-derived neurotrophic factor protein content was reduced in both the olfactory bulbs (-24.6%) and hippocampus (-28.2%) of Prenatally Stressed male offspring at postnatal days 1 and 5, respectively. These detrimental central changes observed may partly explain the increased susceptibility of Prenatally Stressed subjects to mood disorders including depression in later life.
Marta Weinstock - One of the best experts on this subject based on the ideXlab platform.
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perinatal citalopram does not prevent the effect of Prenatal Stress on anxiety depressive like behaviour and serotonergic transmission in adult rat offspring
European Journal of Neuroscience, 2016Co-Authors: Inbar Zohar, Shai Shoham, Marta WeinstockAbstract:It is still not clear whether the selective serotonin reuptake inhibitors frequently prescribed to depressed pregnant women improve the behavioural outcome in their children. The current study investigated whether administration of citalopram to pregnant rats could prevent anxiety and depressive-like behaviour induced by gestational Stress in their offspring, and restore the expression of serotonin 1A autoreceptors in GABAergic interneurons in the medial prefrontal cortex and dorsal raphe nuclei in males, and of corticotropin-releasing factor type 2 receptors in GABAergic interneurons in the dorsal raphe nuclei in females. Activation of these receptors modulates serotonergic transmission to target areas and is reduced in a sex-dependent manner by Prenatal Stress. Citalopram (10 mg/kg/day), administered orally from day 7 of gestation until 21 days postpartum, prevented the increase in anxiety in Stressed mothers but did not reduce anxiety and depressive-like behaviour in their offspring and even induced depressive-like behaviour in the offspring of control mothers. Citalopram failed to restore the reduction in the expression of serotonin 1A autoreceptors in the prefrontal cortex of males and in corticotropin-releasing factor type 2 receptors in the dorsal raphe nuclei of females induced by Prenatal Stress. Prenatal citalopram did not prevent the behavioural changes or reduction in serotonergic transmission to target areas induced by Prenatal Stress. It had adverse behavioural effects in the offspring of control rats, which, together with the lack of any change in Prenatally-Stressed rats, may be due to inhibition of the foetal serotonin transporter thereby preventing normal development of the serotonin system.
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effect of Prenatal Stress on plasma corticosterone and catecholamines in response to footshock in rats
Physiology & Behavior, 1998Co-Authors: Marta Weinstock, Tatyana Poltyrev, Donna Schorerapelbaum, Richard MccartyAbstract:The effect of Prenatal Stress was investigated on the sympathoadrenal response to novelty and footshock by measuring the time course of the changes in circulating corticosterone (COR) catecholamines and their metabolites. Pregnant rats were subjected to noise and light Stress, three times weekly on an unpredictable basis throughout gestation. When the male offspring of Stressed rats (PS) and those of unStressed mothers (C) were 4.5-5 months of age, they were prepared with indwelling catheters in the tail artery 24 h before the experiment. Resting levels of plasma COR, noradrenaline (NA), adrenaline (AD), dihydroxyphenylglycol (DHPG), dihydroxyphenylacetic acid (DOPAC), and dihydroxyphenylalanine (DOPA) were measured. Further blood samples were taken within 3 min of their transfer to the shock box, 1-2, 5, 15, and 45 min after footshock. Plasma COR was significantly higher in PS than in C rats at rest, but those of adrenaline, NA, and their metabolites did not differ in the two groups. Transfer of the rats to the shock box increased plasma COR, NA, adrenaline, and dihydroxyphenylglycol in both groups, and dihydroxyphenylalanine and dihydroxyphenylacetic acid only in PS rats. All the catechols increased further 2-3 min after footshock, except dihydroxyphenylalanine in PS rats. Plasma NA and dihydroxyphenylglycol levels were significantly higher in PS than in C rats immediately after footshock, indicating a greater activation of the sympathetic nervous system in PS rats. The findings demonstrate for the first time that Prenatal Stress can induce long term changes in the sensitivity of the sympathoadrenal system to Stress.
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does Prenatal Stress impair coping and regulation of hypothalamic pituitary adrenal axis
Neuroscience & Biobehavioral Reviews, 1997Co-Authors: Marta WeinstockAbstract:WEINSTOCK, M. Does Prenatal Stress impair coping and regulation of hypothalamic-pituitary-adrenal axis? NEUROSCI BIOBEHAV REV 21(1),1–10 1997.—Prenatally Stressed (PS) human infants and experimental animals show attentional deficits, hyperanxiety and disturbed social behavior. Impaired coping in Stressful situations in adult PS monkeys and rodents is associated with dysregulation of the HPA axis, characterized by decreased feedback inhibition of corticotropin-releasing hormone (CRH) and prolonged elevation of plasma glucocorticoids in response to Stress. PS rats have higher levels of CRH in the amygdala, fewer hippocampal glucocorticoid receptors and less endogenous opioid and GABA/BDZ (benzodiazepine) inhibitory activity. The mechanisms by which maternal Stress hormones induce these long-lasting changes in the developing fetal neuroaxis remain to be elucidated. It is suggested that impaired coping in Stressful situations and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, result from the action of maternal hormones released during Stress on the developing fetus. The similarities in coping behavior and dysregulation of the HPA axis in PS animals to those in humans with depression, suggest that gestational Stress, at a critical time during fetal development, may increase the propensity to develop this condition. Copyright © 1996 Elsevier Science Ltd.
