Chronic immobilization stress: evidence for decreases of 5-hydroxy-tryptamine immunoreactivity and for increases of glucocorticoid receptor immunoreactivity in various brain regions of the male rat

Kitayama, Isao; Cintra, A.; Janson, Ann Marie; Fuxé, Kjell; Agnati, Luigi F.; Eneroth, P.; Aronsson, M.; Härfstrand, Anders; Steinbush, H. W. M.; Visser, Theo J.; Goldstein, Menek; Vale, Wylie; Gustafsson, Jan‐Åke

doi:10.1007/bf01248925

Cited by 39 publications

(9 citation statements)

References 68 publications

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“…In the DRN, a significant increase in GR mRNA levels was observed in CMS-exposed WT mice, in line with previous studies showing an increased GR expression in this nucleus after chronic restraint stress in rats (Kitayama et al, 1989). In GR-i mice also, DRN GR mRNA levels tended to increase (but not significantly) after CMS exposure.…”

Section: Discussionsupporting

confidence: 78%

Neurochemical and Behavioral Alterations in Glucocorticoid Receptor-Impaired Transgenic Mice after Chronic Mild Stress

Froger¹,

Palazzo²,

Boni³

et al. 2004

J. Neurosci.

105

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Mice (GR-i) bearing a transgene encoding a glucocorticoid receptor (GR)antisense RNA under the control of a neuron-specific neurofilament promoter were used to investigate the effects of a 4 week chronic mild stress (CMS) on the hypothalamo-pituitary-adrenocortical (HPA) axis and the serotoninergic system in a transgenic model of vulnerability to affective disorders. GR-i mice showed a decrease in both GR-specific binding (hippocampus and cerebral cortex) and GR mRNA levels [hippocampus, cerebral cortex, and dorsal raphe nucleus (DRN)] as well as a deficit in HPA axis feedback control (dexamethasone test) compared with paired wild-type (WT) mice. In the latter animals, CMS exposure caused a significant decrease in both GR mRNA levels and the density of cytosolic GR binding sites in the hippocampus, whereas, in the DRN, GR mRNA levels tended to increase. In contrast, in stressed GR-i mice, both GR mRNA levels and the density of GR binding sites were significantly increased in the hippocampus, cerebral cortex, and DRN. Electrophysiological recordings in brainstem slices and [␥-35 S]GTP-S binding measurements to assess 5-HT 1A receptor functioning showed that CMS exposure produced a desensitization of DRN 5-HT 1A autoreceptors in WT, but not in GR-i, mice. In addition, CMS was found to facilitate choice behavior of WT, but not GR-i, mice in a decision-making task derived from an alternation paradigm. These results demonstrate that impaired GR functioning affects normal adaptive responses of the HPA axis and 5-HT system to CMS and alters stress-related consequences on decision-making behaviors.

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Section: Discussionsupporting

confidence: 78%

Neurochemical and Behavioral Alterations in Glucocorticoid Receptor-Impaired Transgenic Mice after Chronic Mild Stress

Froger¹,

Palazzo²,

Boni³

et al. 2004

J. Neurosci.

105

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“…Studies performed with ligand binding and quantitative immunocytochemistry techniques indicate that cellular GR levels vary as a result of, e.g., endocrine manipulations (13), stress (14,15), and aging (16,17). By means of an in situ hybridization technique, it has been possible in the present paper to detect and map out the distribution of GR mRNA in the male rat brain.…”

mentioning

confidence: 99%

Localization of glucocorticoid receptor mRNA in the male rat brain by in situ hybridization.

Aronsson

Fuxé

Dong

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

217

111

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The localization and distribution of mRNA encoding the glucocorticoid receptor (GR) was investigated in tissue sections of the adult male rat brain by in situ hybridize. tion and RNA blot analysis. GR mRNA levels were measured by quantitative autoradiography with IS-and 32P-labeled RNA probes, respectively. Strong labeling was observed within the pyramidal nerve cells of the CAl and CA2 areas of the hippocampal formation, in the granular cells of the dentate gyrus, in the parvocellular nerve cells of the paraventricular hypothalamic nucleus, and in the cells of the arcuate nucleus, especially the parvocellular part. Moderate labeling of a large number of nerve cells was observed within layers II, III, and VI of the neocortex and in many thalamic nuclei, especially the anterior and ventral nuclear groups as well as several midline nuclei. Within the cerebellar cortex, strong labeling was observed all over the granular layer. In the lower brainstem, strong labeling was found within the entire locus coeruleus and within the mesencephalic raphe nuclei rich in noradrenaline and 5-hydroxytryptamine cell bodies, respectively. A close correlation was found between the distribution of GR mRNA and the distribution of previously described GR immunoreactivity. These studies open the possibility of obtaining additional information on in vivo regulation of GR synthesis and how the brain may alter its sensitivity to circulating glucocorticoids.Adrenal steroids have a wide range of actions in the central nervous system, where they have been shown to affect growth and differentiation of nerve cells as well as mental state, perception, learning, and sleep (for a review, see ref.1). Glucocorticoids, as well as other steroid hormones, exert at least a part of their action via binding to specific intracellular receptor proteins, acting as modulators of the transcriptional activity of specific networks of genes (for a review, see ref.2). Corticosterone binds to two distinct receptor systems in the rat brain (4)-the mineralocorticoid-receptor-like type I receptor and the classical glucocorticoid receptor (GR). Recently, it has been possible to map out GR immunoreactive nerve cell populations (5-9) and glucocorticoid recognition sites (10, 11) in many areas of the central nervous system by means of mouse monoclonal antibodies against the rat liver GR (12) and specific GR radioligands, respectively. High levels of glucocorticoid binding (11) and strong GR immunoreactivity (5, 8) were found within the monoaminergic neurons, in the hippocampal formation, in the corticotropinreleasing factor immunoreactive neurons, and in the mediobasal hypothalamus.Studies performed with ligand binding and quantitative immunocytochemistry techniques indicate that cellular GR levels vary as a result of, e.g., endocrine manipulations (13), stress (14, 15), and aging (16,17). By means of an in situ hybridization technique, it has been possible in the present paper to detect and map out the distribution of GR mRNA in the male rat brain. These results ...

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“…Glucocorticoids exert central feedback in stress by regulating gene expression. Glucocorticoid signaling is altered in the A1 neurons by chronic stress (Kitayama et al 1989), which may affect the expression of TH, PrRP and nesfatin. The expression of these genes may also be affected by neural inputs modulating the excitability of cells.…”

Section: Discussionmentioning

confidence: 99%

Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia

et al. 2020

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Chronic hypernatremia activates the central osmoregulatory mechanisms and inhibits the function of the hypothalamic-pituitary-adrenal (HPA) axis. Noradrenaline (NE) release into the periventricular anteroventral third ventricle region (AV3V), the supraoptic (SON) and hypothalamic paraventricular nuclei (PVN) from efferents of the caudal ventrolateral (cVLM) and dorsomedial (cDMM) medulla has been shown to be essential for the hypernatremia-evoked responses and for the HPA response to acute restraint. Notably, the medullary NE cell groups highly coexpress prolactin-releasing peptide (PrRP) and nesfatin-1/NUCB2 (nesfatin), therefore, we assumed they contributed to the reactions to chronic hypernatremia. To investigate this, we compared two models: homozygous Brattleboro rats with hereditary diabetes insipidus (DI) and Wistar rats subjected to chronic high salt solution (HS) intake. HS rats had higher plasma osmolality than DI rats. PrRP and nesfatin mRNA levels were higher in both models, in both medullary regions compared to controls. Elevated basal tyrosine hydroxylase (TH) expression and impaired restraint-induced TH, PrRP and nesfatin expression elevations in the cVLM were, however, detected only in HS, but not in DI rats. Simultaneously, only HS rats exhibited classical signs of chronic stress and severely blunted hormonal reactions to acute restraint. Data suggest that HPA axis responsiveness to restraint depends on the type of hypernatremia, and on NE capacity in the cVLM. Additionally, NE and PrRP signalization primarily of medullary origin is increased in the SON, PVN and AV3V in HS rats. This suggests a cooperative action in the adaptation responses and designates the AV3V as a new site for PrRP's action in hypernatremia.

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Chronic immobilization stress: evidence for decreases of 5-hydroxy-tryptamine immunoreactivity and for increases of glucocorticoid receptor immunoreactivity in various brain regions of the male rat

Cited by 39 publications

References 68 publications

Neurochemical and Behavioral Alterations in Glucocorticoid Receptor-Impaired Transgenic Mice after Chronic Mild Stress

Neurochemical and Behavioral Alterations in Glucocorticoid Receptor-Impaired Transgenic Mice after Chronic Mild Stress

Localization of glucocorticoid receptor mRNA in the male rat brain by in situ hybridization.

Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia

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