Prenatal stress and neonatal rat brain development

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 inve...

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Published inNeuroscience Vol. 137; no. 1; pp. 145 - 155
Main Authors Van den Hove, D.L.A., Steinbusch, H.W.M., Scheepens, A., Van de Berg, W.D.J., Kooiman, L.A.M., Boosten, B.J.G., Prickaerts, J., Blanco, C.E.
Format Journal Article
LanguageEnglish
Published Oxford Elsevier Ltd 2006
Elsevier
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Abstract 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.
AbstractList 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.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.
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.
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.
Author Steinbusch, H.W.M.
Van de Berg, W.D.J.
Scheepens, A.
Boosten, B.J.G.
Van den Hove, D.L.A.
Prickaerts, J.
Blanco, C.E.
Kooiman, L.A.M.
Author_xml – sequence: 1
  givenname: D.L.A.
  surname: Van den Hove
  fullname: Van den Hove, D.L.A.
  email: d.vandenhove@np.unimaas.nl
  organization: Department of Pediatrics, Research Institute Growth and Development, Faculty of Medicine, Maastricht University, P. Debyelaan 25, P. O. Box 5800, 6202 AZ, Maastricht, The Netherlands
– sequence: 2
  givenname: H.W.M.
  surname: Steinbusch
  fullname: Steinbusch, H.W.M.
  organization: Department of Psychiatry and Neuropsychology, Division of Neuroscience, European Graduate School of Neuroscience, Faculty of Medicine, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands
– sequence: 3
  givenname: A.
  surname: Scheepens
  fullname: Scheepens, A.
  organization: Department of Pediatrics, Research Institute Growth and Development, Faculty of Medicine, Maastricht University, P. Debyelaan 25, P. O. Box 5800, 6202 AZ, Maastricht, The Netherlands
– sequence: 4
  givenname: W.D.J.
  surname: Van de Berg
  fullname: Van de Berg, W.D.J.
  organization: Department of Pediatrics, Research Institute Growth and Development, Faculty of Medicine, Maastricht University, P. Debyelaan 25, P. O. Box 5800, 6202 AZ, Maastricht, The Netherlands
– sequence: 5
  givenname: L.A.M.
  surname: Kooiman
  fullname: Kooiman, L.A.M.
  organization: Department of Psychiatry and Neuropsychology, Division of Neuroscience, European Graduate School of Neuroscience, Faculty of Medicine, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands
– sequence: 6
  givenname: B.J.G.
  surname: Boosten
  fullname: Boosten, B.J.G.
  organization: Department of Psychiatry and Neuropsychology, Division of Neuroscience, European Graduate School of Neuroscience, Faculty of Medicine, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands
– sequence: 7
  givenname: J.
  surname: Prickaerts
  fullname: Prickaerts, J.
  organization: Department of Psychiatry and Neuropsychology, Division of Neuroscience, European Graduate School of Neuroscience, Faculty of Medicine, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands
– sequence: 8
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  surname: Blanco
  fullname: Blanco, C.E.
  organization: Department of Pediatrics, Research Institute Growth and Development, Faculty of Medicine, Maastricht University, P. Debyelaan 25, P. O. Box 5800, 6202 AZ, Maastricht, The Netherlands
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ISSN 0306-4522
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Issue 1
Keywords brain derived neurotrophic factor
PS
cell proliferation
BDNF
E
pregnancy
P
hypothalamo–pituitary–adrenal axis
OB
ANOVA
SVZ
HPA
depression
LSD
3H-Thy
caspase-3
Human
Cell proliferation
Rat
Hypothalamohypophysoadrenal axis
Enzyme
Cysteine endopeptidases
Rodentia
Central nervous system
Stress
Encephalon
Pregnancy
Prenatal
Peptidases
Vertebrata
Mammalia
Newborn
Animal
Development
Hydrolases
Brain derived neurotrophic factor
hypothalamo-pituitary-adrenal axis
Language English
License https://www.elsevier.com/tdm/userlicense/1.0
CC BY 4.0
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MergedId FETCHMERGED-LOGICAL-c467t-41c426ef9a5a69bd9e5cbfe6275315645a780a753a8a250d0e90fa9fab1f6fec3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
PMID 16242847
PQID 67611666
PQPubID 23479
PageCount 11
ParticipantIDs proquest_miscellaneous_67611666
pubmed_primary_16242847
pascalfrancis_primary_17461780
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elsevier_clinicalkey_doi_10_1016_j_neuroscience_2005_08_060
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PublicationTitle Neuroscience
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Publisher Elsevier Ltd
Elsevier
Publisher_xml – name: Elsevier Ltd
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SubjectTerms Animals
Biological and medical sciences
Brain - embryology
Brain - metabolism
brain derived neurotrophic factor
Brain-Derived Neurotrophic Factor - metabolism
Caspase 3
Caspases - metabolism
Cell Proliferation
Corticosterone - blood
depression
Development. Senescence. Regeneration. Transplantation
Female
Fetal Development - physiology
Fundamental and applied biological sciences. Psychology
hypothalamo–pituitary–adrenal axis
Male
Pregnancy
Prenatal Exposure Delayed Effects
Rats
Rats, Inbred F344
Restraint, Physical - adverse effects
Stress, Psychological - physiopathology
Vertebrates: nervous system and sense organs
Title Prenatal stress and neonatal rat brain development
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https://dx.doi.org/10.1016/j.neuroscience.2005.08.060
https://www.ncbi.nlm.nih.gov/pubmed/16242847
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