Central LPS-Induced &lt;i&gt;c-fos&lt;/i&gt; Expression in the PVN and the A1/A2 Brainstem Noradrenergic Cell Groups Is Altered by Adrenalectomy

Conde, Gillian; Renshaw, Derek; Zubelewicz, B; Lightman, Stafford L.; Harbuz, Michael S.

doi:10.1159/000054474

Cited by 16 publications

(13 citation statements)

References 49 publications

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“…Concerning CRH mRNA production in the PVN, our results confirm the existence of a negative glucocorticoid control [40] . Probably as a consequence of the chronic corticosterone feedback discussed above, PVN CRH mRNA levels in the (non-LPS-treated) ADX+cort rats are lower than in the (non-LPS-treated) intact rats.…”

Section: Discussionsupporting

confidence: 74%

Glucocorticoids Down-Regulate Lipopolysaccharide-Induced de novo Production of Neurotensin mRNA in the Rat Hypothalamic, Paraventricular, Corticotrophin-Releasing Hormone Neurons

Loum-Ribot¹,

Lafon²,

Chaigniau³

et al. 2006

Neuroimmunomodulation

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Objective: Intraperitoneal injection of the endotoxin lipopolysaccharide (LPS) produces inflammation accompanied by activation of the immune system and the secretion of cytokines. Cytokines stimulate the hypothalamo-pituitary-adrenal (HPA) axis to release the anti-inflammatory corticosterone which controls its own production by acting on the HPA axis. Upstream in the HPA axis are neuroendocrine corticotrophin-releasing hormone (CRH) neurons located in the paraventricular nucleus (PVN), whose multipeptidergic phenotype changes during inflammation: while CRH mRNA is up-regulated in these conditions, neurotensin (NT) mRNA expression is induced de novo. The negative feedback control of glucocorticoids on CRH production is well documented; however, their action on NT production in the PVN of the hypothalamus is poorly documented. The aim of this study was to determine if glucocorticoids modulate the de novo production of NT during inflammation. Methods: Using quantitative in situ hybridization histochemistry, we examined whether the absence (adrenalectomy) or excess (corticosterone implants) of glucocorticoids modulate de novo production of NT mRNA in the PVN during inflammation induced by LPS treatment. Results: A relatively low dose of LPS (50 µg/kg) that is not efficient to induce NT mRNA production in the PVN becomes efficient after adrenalectomy. Moreover, corticosterone excess reduces LPS-induced production of NT mRNA in the PVN. Conclusion: Glucocorticoids exert a negative control on NT mRNA production in the PVN of the hypothalamus, and this effect requires that NT mRNA production be triggered, such as during inflammation.

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Section: Discussionsupporting

confidence: 74%

Glucocorticoids Down-Regulate Lipopolysaccharide-Induced de novo Production of Neurotensin mRNA in the Rat Hypothalamic, Paraventricular, Corticotrophin-Releasing Hormone Neurons

Loum-Ribot¹,

Lafon²,

Chaigniau³

et al. 2006

Neuroimmunomodulation

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“…This dose of LPS of the 055:B5 serotype is sufficient to stimulate the HPA axis with no apparent effects on animal behaviour, e.g., locomotion, fur appearance, exploratory behaviour (Conde et al, 1999). Twenty-one days later, both groups of animals were injected i.p.…”

Section: Methodsmentioning

confidence: 99%

Re-exposure to endotoxin induces differential cytokine gene expression in the rat hypothalamus and spleen

Rey¹,

Randolf²,

Wildmann³

et al. 2009

Brain, Behavior, and Immunity

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This study was designed to investigate whether the pattern of hypothalamic and splenic cytokine expression induced by peripheral administration of a bacterial lipopolysaccharide (LPS) is affected by prior exposure to LPS derived from another bacterial strain. Injection of LPS from Salmonella enteritidis (LPS2) alone resulted in increased hypothalamic gene expression of IL-1β, IL-6, TNFα, IL-1ra and IL-10. However, pre-exposure to LPS derived from Escherichia coli (LPS1) 3 weeks before, significantly attenuated hypothalamic IL-1ra, IL-6 and IL-10 expression. IL-1β expression also tended to be lower. This pattern contrasted with the robust cytokine expression in the spleen of LPS2-treated rats previously exposed to LPS1, since pre-treatment with endotoxin resulted in a significantly greater response of IL-1β and IL-1ra to LPS2. Expression of TNFα and IL-10 also tended to be higher. Pre-treatment with LPS1 did not significantly affect the marked increase in corticosterone and adrenaline blood levels induced by LPS2. Thus, while endotoxin pre-exposure seemed not to induce a “tolerant” state in the periphery as judged by the immune and endocrine parameters evaluated upon re-stimulation, expression of four of the six cytokines measured was decreased in the hypothalamus. This is the first demonstration that endotoxin priming can differentially affect cytokine expression in the central nervous system and peripheral tissues when a host is confronted with a second, acute, pro-inflammatory stimulus. These results may provide new evidence for the involvement of cytokine pathways in the central nervous system in modulating peripheral inflammation and mediating cognitive and behavioural alterations during inflammatory diseases.

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“…Trunk blood, brains and pituitaries were collected. We have previously demonstrated LPS-induced increases in CRH mRNA using this serotype (Escherichia coli; 055:B5) at the 3-h time point (20).…”

Section: Sampling Proceduresmentioning

confidence: 95%

Gonadectomy Reverses The Sexually Diergic Patterns Of Circadian and Stress‐Induced Hypothalamic‐Pituitary‐Adrenal Axis Activity In Male and Female Rats

Seale

Wood

Atkinson

et al. 2004

J Neuroendocrinology

214

126

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Enhanced corticosterone release by female compared to male rats under basal and stress conditions is well documented. The demonstration that gonadectomy enhances stress-induced corticosterone secretion in male rats, but reduces such levels in female rats, suggests a causal association between gonadal steroids and corticosterone release. The present study examined the corticosterone profile of sham gonadectomized and gonadectomized female and male rats under basal and stress conditions. An automated sampling system collected blood from each freely moving, unanaesthetized rat every 10 min (i) over a 24-h period; (ii) following noise stress; and (iii) following an immune-mediated stress (lipopolysaccharide, LPS). Plasma was analysed for corticosterone content using radioimmunoassay. Castration resulted in a significant increase in basal corticosterone release compared to the sham-castrated male rats. Pulsar analysis revealed a significant two-fold increase in the number of corticosterone pulses over 24 h. Corticosterone increases in response to noise stress and to LPS injection were enhanced following castration. Conversely, ovariectomy resulted in a two-fold reduction in the number of corticosterone pulses as well as the stress response compared to sham-ovariectomized female rats. Arginine vasopressin (AVP), corticotrophin-releasing hormone (CRH) and glucocorticoid receptor mRNAs in the paraventricular nucleus and pro-opiomelanocortin (POMC) mRNA in the anterior pituitary were analysed post-LPS administration by in situ hybridization. Significantly higher values were found for AVP, CRH and POMC mRNAs examined for sham females and castrated males compared to sham males and ovariectomized females. This study confirms previous reports concerning the influence of gonadal factors in regulating HPA axis activity and stress responsiveness. The present results extend these observations to the regulation of the dynamic pattern of corticosterone release under basal conditions and suggests that this alteration in pulsatility is important for the differences in stress responsiveness when comparing males and females.

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Central LPS-Induced <i>c-fos</i> Expression in the PVN and the A1/A2 Brainstem Noradrenergic Cell Groups Is Altered by Adrenalectomy

Cited by 16 publications

References 49 publications

Glucocorticoids Down-Regulate Lipopolysaccharide-Induced de novo Production of Neurotensin mRNA in the Rat Hypothalamic, Paraventricular, Corticotrophin-Releasing Hormone Neurons

Glucocorticoids Down-Regulate Lipopolysaccharide-Induced de novo Production of Neurotensin mRNA in the Rat Hypothalamic, Paraventricular, Corticotrophin-Releasing Hormone Neurons

Re-exposure to endotoxin induces differential cytokine gene expression in the rat hypothalamus and spleen

Gonadectomy Reverses The Sexually Diergic Patterns Of Circadian and Stress‐Induced Hypothalamic‐Pituitary‐Adrenal Axis Activity In Male and Female Rats

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