The effects of prenatal stress on the Purkinje cell neurogenesis

Ulupinar, Emel; Yücel, Ferruh; Ortug, Gursel

doi:10.1016/j.ntt.2005.10.003

Cited by 35 publications

(35 citation statements)

References 65 publications

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“…Interestingly, these results are different from those in animal models of gestational stress. When pregnant Sprague-Dawley rats were restrained for 6 h on GD 7 and 14, the resultant offspring actually had an increase in Purkinje cell density and volume [22] . Animal models of fetal alcohol syndrome have also shown that ethanol consumption during pregnancy decreases Purkinje cell density and responsiveness, as do animal models being administered ␤ 2 -adrenoceptor agonists in the earlier postnatal period [23,24] .…”

Section: Discussionmentioning

confidence: 99%

Prenatal Infection Decreases Calbindin, Decreases Purkinje Cell Volume and Density and Produces Long-Term Motor Deficits in Sprague-Dawley Rats

et al. 2010

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The cerebellum is involved in the control of motor functions with Purkinje cells serving as the only output from the cerebellum. Purkinje cells are important targets for toxic substances and are vulnerable to prenatal insults. Intrauterine infection (IUI) has been shown to selectively target the developing cerebral white matter through lesioning, necrosis and inflammatory cytokine activation. Developmental and cognitive delays have been associated with animal models of IUI. The aim of this study was to determine if IUI leads to damage to Purkinje cells in the developing cerebellum and if any damage is associated with decreases in calbindin and motor behaviors in surviving pups. Pregnant rats were injected with Escherichia coli (1 × 10⁵ colony-forming units) or sterile saline at gestational day 17. Beginning at postnatal day (PND) 2, the pups were subjected to a series of developmental tests to examine developmental milestones. At PND 16, some pups were sacrificed and their brains extracted and processed for histology or protein studies. Hematoxylin and eosin (HE) staining was done to examine the general morphology of the Purkinje cells and to examine Purkinje cell density, area and volume. Calbindin expression was examined in the cerebellum via immunohistochemistry and Western blot techniques. The remaining rat pups were used to examine motor coordination and balance on a rotating rotarod at the prepubertal and adult ages. Prenatal E. coli injection did not significantly change birth weight or delivery time, but did delay surface righting and negative geotaxis in pups. Pups in the E. coli group also had a decrease in the number of Purkinje cells, as well as a decrease in Purkinje cell density and volume. HE staining demonstrated a change in Purkinje cell morphology. Calbindin expression was decreased in rats from the E. coli group as well. Locomotor tests indicated that while there were no significant changes in gross motor activity, motor coordination and balance was impaired in both prepubertal and adult rats from the E. coli group. In this model of IUI, we observed changes in Purkinje cell development which were associated with alterations in cerebellum-dependent motor behaviors. The decreases in calbindin and Purkinje cells were associated with developmental delays. These data further support the importance of IUI in brain development.

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Section: Discussionmentioning

confidence: 99%

Prenatal Infection Decreases Calbindin, Decreases Purkinje Cell Volume and Density and Produces Long-Term Motor Deficits in Sprague-Dawley Rats

et al. 2010

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“…In Übereinstimmung mit der Funktion des Hippokampus für Gedächtnis und Verhalten sind die strukturellen Störungen des Hippokampus mit kognitiven Störungen und Verhaltensauffälligkeiten im spä-teren Leben assoziiert [189] . Diese funktionellen Stö-rungen spiegeln sich in einem gestörten neuronalen Netzwerk wider [188,[190][191][192][193][194] .…”

Section: Mechanismen Der Effekte Von Pränatalem Stress Und Einer Pränunclassified

“…Auf struktureller Ebene geht die pränatal programmierte Hyperaktivität der HHN-Achse im späteren Leben mit einer verminderten Ausschüttung von Wachstumsfaktoren [186] und einer Hemmung der Neuroneogenese bis hin zur neuronalen Degeneration einher [169,188,189,193,194] . Interessanterweise gehen stressbedingte Erkrankungen wie die posttraumatische Belastungsstörung [195] oder Depressionen [196,197] beim Menschen mit den gleichen strukturellen Veränderungen im Hippokampus wie pränatal erhöhte Glukokortikoidspiegel einher, wobei wahrscheinlich auch hier erhöhte Kortisolspiegel eine pathogenetisch entscheidende Rolle spielen.…”

Section: Mechanismen Der Effekte Von Pränatalem Stress Und Einer Pränunclassified

“…Hierfür spielt eine Resistenz von Glukokortikoidrezeptoren im Immunsystem gegenüber den immunmodulatorischen Effekten von Kortisol eine Rolle. Neben diesen Effekten sind wahrscheinlich auch andere, durch pränatal erhöhte Glukokortikoidspiegel «programmierte» Effekte wie eine Störung der Neuroneogenese wesentlich [188,189,193,194] .…”

Section: Programmierung Zerebrovaskulärer Erkrankungenunclassified

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Intrauterine Programmierung von Störungen der Hirnfunktion im späteren Leben

Schwab¹

2009

Gynäkol Geburtshilfliche Rundsch

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Die Entwicklung der Hirnfunktion wird pränatal durch epigenetische Faktoren, die insbesondere mit einer fetalen Mangelversorgung oder erhöhten fetalen Stresshormonkonzentrationen einhergehen, beeinflusst. Schon eine moderate Mangelernährung hat Effekte auf die Hirnentwicklung u.a. über eine Hemmung des Systems des insulinähnlichen Wachstumsfaktors. Daneben führt sie zu einer Erhöhung von mütterlichen Kortisolkonzentrationen im fetalen Kreislauf. Erhöhte fetale Kortisolkonzentrationen, sei es aufgrund fetaler Mangelversorgung, Stress oder pränataler Gabe von Glukokortikoiden, führen ebenfalls zu Störungen der Hirnentwicklung. Darüber hinaus induzieren sie in den letzten Wochen der Schwangerschaft, wenn die kindliche Hypophysen-Hypothalamus-Nebennieren-(HHN)-Achse reift, eine dauerhafte Desensitivierung von Glukokortikoidrezeptoren im Hippokampus. Diese bewirkt eine verminderte negative Rückkopplung der HHN-Achse mit der Folge einer verstärkten Kortisolausschüttung und einer erhöhten Stressempfindlichkeit im späteren Leben. Die Störungen der Hirnentwicklung und die dauerhaft erhöhten Kortisolspiegel induzieren subtile kognitive Störungen, Verhaltensauffälligkeiten und eine Prädisposition für depressive und schizophrene Erkrankungen.

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“…These regions include the hippocampus [53][54][55][56][57] , amygdala [58][59][60] , corpus callosum 61 , cerebral cortex 62,63 , cerebellum 64,65 and hypothalamus 66,67 . Since morphological changes in the above brain regions have been linked with certain psychological and behavioural problems, it is possible that prenatal stress affects the neurodevelopmental formation of these areas.…”

Section: Microscopic and Macroscopic Changes In The Brainmentioning

confidence: 99%

Os efeitos do estresse na função do eixo hipotalâmico-pituitário-adrenal em indivíduos com esquizofrenia

Guest

Martins-de-Souza²,

Rahmoune

et al. 2012

Arch. Clin. Psychiatry (São Paulo)

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Over the last few decades, evidence has been emerging that the pathogenesis of psychiatric disorders such as schizophrenia can involve perturbations of the hypothalamic-pituitary-adrenal (HPA) axis. Variations in the manifestation of these effects could be related to the differences in clinical symptoms between affected individuals as well as to differences in treatment response. Such effects can also arise from the complex interaction between genes and environmental factors. Here, we review the effects of maternal stress on abnormalities in HPA axis regulation and the development of psychiatric disorders including schizophrenia. Studies in this area may prove critical for increasing our understanding of the multi-dimensional nature of schizophrenia. Further research in this area could ultimately lead to the development of improved diagnostics and novel therapeutic approaches for treating this debilitating psychiatric condition.Guest FL, et al. / Rev Psiq Clín. 2013;40(1):20-7 Keywords: Psychiatric disorders, schizophrenia, HPA axis dysfunction, diagnosis, biomarkers. ResumoNas últimas décadas, têm surgido evidências sugerindo que a patogênese de desordens psiquiátricas, tais como a esquizofrenia, pode envolver perturbações no eixo hipotalâmico-pituitário-adrenal (HPA). Variações na manifestação desses efeitos poderiam estar relacionadas a diferenças em sintomas clínicos entre os indivíduos afetados, assim como a diferenças na resposta ao tratamento. Tais efeitos podem também ser originados de complexas interações entre genes e fatores ambientais. Aqui, revisamos os efeitos do estresse maternal em anormalidades na regulação do eixo HPA e desenvolvimento de desordens psiquiátricas, incluindo a esquizofrenia. Estudos nessa área podem gerar o aumento do nosso entendimento da natureza multidimensional da esquizofrenia. Posterior pesquisa nesse campo poderia, em última instância, levar ao desenvolvimento de melhores diagnósticos e novas abordagens terapêuticas para essa debilitante condição psiquiátrica.Guest FL, et al. / Rev Psiq Clín. 2013;40(1):20-7 Palavras-chave: Desordens psiquiátricas, esquizofrenia, disfunção do eixo HPA, diagnóstico, biomarcadores.

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The effects of prenatal stress on the Purkinje cell neurogenesis

Cited by 35 publications

References 65 publications

Prenatal Infection Decreases Calbindin, Decreases Purkinje Cell Volume and Density and Produces Long-Term Motor Deficits in Sprague-Dawley Rats

Prenatal Infection Decreases Calbindin, Decreases Purkinje Cell Volume and Density and Produces Long-Term Motor Deficits in Sprague-Dawley Rats

Intrauterine Programmierung von Störungen der Hirnfunktion im späteren Leben

Os efeitos do estresse na função do eixo hipotalâmico-pituitário-adrenal em indivíduos com esquizofrenia

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