Prenatal stress alters Fos protein expression ...
Document type :
Article dans une revue scientifique: Article original
PMID :
Permalink :
Title :
Prenatal stress alters Fos protein expression in hippocampus and locus coeruleus stress-related brain structures
Author(s) :
Viltart, Odile [Auteur]
Université de Lille, Sciences et Technologies
Mairesse, Jérôme [Auteur]
Darnaudéry, Muriel [Auteur]
Louvart, Hélène [Auteur]
Vanbesien-Mailliot, Christel [Auteur]
Catalani, Assia [Auteur]
Maccari, Stefania [Auteur]
Université de Lille, Sciences et Technologies
Università degli Studi di Roma "La Sapienza" = Sapienza University [Rome] [UNIROMA]
Université de Lille, Sciences et Technologies
Mairesse, Jérôme [Auteur]
Darnaudéry, Muriel [Auteur]
Louvart, Hélène [Auteur]
Vanbesien-Mailliot, Christel [Auteur]
Catalani, Assia [Auteur]
Maccari, Stefania [Auteur]
Université de Lille, Sciences et Technologies
Università degli Studi di Roma "La Sapienza" = Sapienza University [Rome] [UNIROMA]
Journal title :
Psychoneuroendocrinology
Volume number :
31
Pages :
769-80
Publication date :
2006-07-01
ISSN :
0306-4530
English keyword(s) :
Animals
Corticosterone
Female
Hippocampus
Hypothalamo-Hypophyseal System
Locus Coeruleus
Male
Neurons
Paraventricular Hypothalamic Nucleus
Pregnancy
Prenatal Exposure Delayed Effects
Proto-Oncogene Proteins c-fos
Rats
Stress, Psychological
Tissue Distribution
Vesicular Inhibitory Amino Acid Transport Proteins
Corticosterone
Female
Hippocampus
Hypothalamo-Hypophyseal System
Locus Coeruleus
Male
Neurons
Paraventricular Hypothalamic Nucleus
Pregnancy
Prenatal Exposure Delayed Effects
Proto-Oncogene Proteins c-fos
Rats
Stress, Psychological
Tissue Distribution
Vesicular Inhibitory Amino Acid Transport Proteins
HAL domain(s) :
Sciences cognitives
English abstract : [en]
Prenatal stress (PS) durably influences responses of rats from birth throughout life by inducing deficits of the hypothalamo-pituitary-adrenal (HPA) axis feedback. The neuronal mechanisms sustaining such alterations are ...
Show more >Prenatal stress (PS) durably influences responses of rats from birth throughout life by inducing deficits of the hypothalamo-pituitary-adrenal (HPA) axis feedback. The neuronal mechanisms sustaining such alterations are still unknown. The purpose of the present study was to determine whether in PS and control rats, the exposure to a mild stressor differentially induces Fos protein in hippocampus and locus coeruleus, brain areas involved in the feedback control of the HPA axis. Moreover, Fos protein expression was also evaluated in the hypothalamic paraventricular nucleus (PVN) that reflect the magnitude of the hormonal response to stress. Basal plasma corticosterone levels were not different between the groups, while, PS rats exhibited higher number of Fos-immunoreactive neurons than controls, in the hippocampus and locus coeruleus in basal condition. A higher basal expression of a marker of GABAergic synapses, the vGAT, was also observed in the hypothalamus of PS rats. Fifteen minutes after the end of the exposure to the open arm of the elevated plus-maze (mild stress) a similar increased plasma corticosterone levels was observed in both groups in parallel with an increased number of Fos-immunoreactive neurons in the PVN. Return to basal plasma corticosterone values was delayed only in the PS rats. On the contrary, after stress, no changes in Fos-immunoreactivity were observed in the hippocampus and locus coeruleus of PS rats compared to basal condition. After stress, only PS rats presented an elevation of the number of activated catecholaminergic neurons in the locus coeruleus. In conclusion, these results suggest for the first time that PS alters the neuronal activation of hippocampus and locus coeruleus implicated in the feedback mechanism of the HPA axis. These data give anatomical substrates to sustain the HPA axis hyperactivity classically described in PS rats after stress exposure.Show less >
Show more >Prenatal stress (PS) durably influences responses of rats from birth throughout life by inducing deficits of the hypothalamo-pituitary-adrenal (HPA) axis feedback. The neuronal mechanisms sustaining such alterations are still unknown. The purpose of the present study was to determine whether in PS and control rats, the exposure to a mild stressor differentially induces Fos protein in hippocampus and locus coeruleus, brain areas involved in the feedback control of the HPA axis. Moreover, Fos protein expression was also evaluated in the hypothalamic paraventricular nucleus (PVN) that reflect the magnitude of the hormonal response to stress. Basal plasma corticosterone levels were not different between the groups, while, PS rats exhibited higher number of Fos-immunoreactive neurons than controls, in the hippocampus and locus coeruleus in basal condition. A higher basal expression of a marker of GABAergic synapses, the vGAT, was also observed in the hypothalamus of PS rats. Fifteen minutes after the end of the exposure to the open arm of the elevated plus-maze (mild stress) a similar increased plasma corticosterone levels was observed in both groups in parallel with an increased number of Fos-immunoreactive neurons in the PVN. Return to basal plasma corticosterone values was delayed only in the PS rats. On the contrary, after stress, no changes in Fos-immunoreactivity were observed in the hippocampus and locus coeruleus of PS rats compared to basal condition. After stress, only PS rats presented an elevation of the number of activated catecholaminergic neurons in the locus coeruleus. In conclusion, these results suggest for the first time that PS alters the neuronal activation of hippocampus and locus coeruleus implicated in the feedback mechanism of the HPA axis. These data give anatomical substrates to sustain the HPA axis hyperactivity classically described in PS rats after stress exposure.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Administrative institution(s) :
Université de Lille
CNRS
CHU Lille
CNRS
CHU Lille
Collections :
Submission date :
2024-01-12T14:49:22Z
2024-02-28T09:53:15Z
2024-02-28T09:53:15Z
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