Bacterial translocation can increase plasma corticosterone and brain catecholamine and indoleamine metabolism

2000 ◽  
Vol 279 (6) ◽  
pp. R2164-R2172 ◽  
Author(s):  
Tetsuya Ando ◽  
Rhonda F. Brown ◽  
Rodney D. Berg ◽  
Adrian J. Dunn
Keyword(s):  
Hpa Axis ◽  
Bacterial Translocation ◽  
Plasma Corticosterone ◽  
Potential Contribution ◽  
Mesenteric Lymph Nodes ◽  
Gram Positive Bacteria ◽  
Amine Metabolism ◽  
Viable Bacteria ◽  
Neurochemical Changes ◽  
Indoleamine Metabolism

The potential contribution of stress-induced bacterial translocation to the activation of the hypothalamo-pituitary-adrenocortical (HPA) axis and brain biogenic amines was assessed. Mice were restrained for various periods, and brain concentrations of tryptophan, catecholamines, serotonin, and their metabolites, plasma corticosterone, and the translocation of viable bacteria from the gastrointestinal tract to the mesenteric lymph nodes, spleen, and liver were measured. Restraint induced the translocation of indigenous gram-positive bacteria in only a small proportion of animals, but translocation of gram-negative bacteria did not occur. Restraint induced short-lived increases in plasma corticosterone and brain amine metabolism, whereas bacterial translocation was slower and persisted long after the HPA axis and neurochemical responses had dissipated. When mice were infected with Salmonella typhimurium, spontaneous translocation occurred and plasma corticosterone, interleukin-6 concentrations, and brain catecholamine and indoleamine metabolism were elevated. These findings indicate that the translocation of indigenous gastrointestinal bacteria did not contribute to the HPA axis and neurochemical changes induced by restraint. However, translocation of nonindigenous S. typhimurium with or without restraint did induce HPA and neurochemical responses.

scholarly journals Behavioural and neurochemical changes induced by stress-related conditions are counteracted by the neurokinin-2 receptor antagonist saredutant

2013 ◽  
Vol 16 (4) ◽  
pp. 813-823 ◽  
Author(s):  
Alessandra Tamburella ◽  
Gian Marco Leggio ◽  
Vincenzo Micale ◽  
Andrea Navarria ◽  
Claudio Bucolo ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Hpa Axis ◽  
Forced Swim Test ◽  
Plasma Corticosterone ◽  
Bdnf Expression ◽  
Immobility Time ◽  
Male Wistar Rats ◽  
Neurochemical Changes ◽  
Nk2 Receptor ◽  
Hpa Axis Activity

Abstract These experiments were undertaken to assess the mechanisms underlying the antidepressant-like effects of the neurokinin-2 (NK2) receptor antagonist saredutant (SR48968) in rats tested in the forced swim test (FST), by analysing hippocampal brain-derived neurotrophic factor (BDNF) and plasma corticosterone [as index of hypothalamic-pituitary-adrenal (HPA) axis activity]. Male Wistar rats received three intraperitoneal injections over 24 h of vehicle, saredutant (5 mg/kg), citalopram (15 mg/kg), clomipramine (50 mg/kg). Rats were subjected to restraint stress (4 h) 24 h prior to the FST procedure. This stress procedure increased immobility and decreased swimming behaviour in the FST; furthermore, it lowered hippocampal BDNF protein expression and increased plasma corticosterone levels. Saredutant and clomipramine or citalopram, used here as positive controls, reduced the immobility time in the FST both under basal conditions and after stress exposure. This effect was not attributable to changes in locomotion, because locomotor activity was unchanged when assessed in the open field test. Pretreatment with para-cholorophenylalanine (150 mg/kg, 72 h and 48 h prior to FST) abolished the effect of citalopram and saredutant on immobility time. At neurochemical level, saredutant attenuated activation of HPA axis in stressed animals more than clomipramine or citalopram. The behavioural effects of saredutant support the hypothesis that NK2 receptor activity is involved in stress-related disorders. These effects of saredutant may be related to normalization of the HPA axis. Moreover, saredutant increases BDNF expression in the hippocampus, confirming the role of NK2 receptor blockade in BDNF activation following stressor application.

scholarly journals Changes in prolactin secretion in the short- and long-term after adrenalectomy

2012 ◽  
Vol 56 (4) ◽  
pp. 244-249 ◽  
Author(s):  
Maria Thereza C. Laguna-Abreu ◽  
Carla Germano ◽  
Ayrton C. Moreira ◽  
José Antunes-Rodrigues ◽  
Lucila Elias ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Plasma Corticosterone ◽  
Prolactin Secretion ◽  
Plasma Prolactin ◽  
Peptidergic Neurons ◽  
Prolactin Release ◽  
Short And Long Term ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

OBJECTIVE: To evaluate the modulation of the hypothalamus-pituitary-adrenal axis (HPA) on prolactin secretion in rats after adrenalectomy (ADX). MATERIALS AND METHODS: Plasma corticosterone, ACTH, and prolactin concentrations were measured by radioimmunoassay in rats after bilateral ADX in the short- (3 hours and 1day) and long-term (3, 7, and 14 days). RESULTS: Animals that underwent ADX showed undetectable corticosterone levels and a triphasic ACTH response with a transient increase (3h), a decrease (1d), and further increase in the long-term after ADX. Sham animals showed a marked increase in corticosterone and ACTH levels three hours after surgery, with a decrease to basal levels thereafter. Plasma prolactin levels were not changed after ADX. CONCLUSION: There are different points of equilibrium in the HPA axis after the glucocorticoid negative feedback is removed. Prolactin plasma secretion is not altered in the short or long- term after ADX, suggesting that the peptidergic neurons essential for prolactin release are not activated after ADX.

scholarly journals Involvement of Neuropeptide Y Y1 Receptors in the Regulation of Neuroendocrine Corticotropin-Releasing Hormone Neuronal Activity

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3666-3673 ◽  
Author(s):  
Eugene L. Dimitrov ◽  
M. Regina DeJoseph ◽  
Mark S. Brownfield ◽  
Janice H. Urban
Keyword(s):  
Neuropeptide Y ◽  
Hpa Axis ◽  
Binding Protein ◽  
Plasma Corticosterone ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Y1 Receptor ◽  
Element Binding Protein ◽  
Y1 Receptors

The neuroendocrine parvocellular CRH neurons in the paraventricular nucleus (PVN) of the hypothalamus are the main integrators of neural inputs that initiate hypothalamic-pituitary-adrenal (HPA) axis activation. Neuropeptide Y (NPY) expression is prominent within the PVN, and previous reports indicated that NPY stimulates CRH mRNA levels. The purpose of these studies was to examine the participation of NPY receptors in HPA axis activation and determine whether neuroendocrine CRH neurons express NPY receptor immunoreactivity. Infusion of 0.5 nmol NPY into the third ventricle increased plasma corticosterone levels in conscious rats, with the peak of hormone levels occurring 30 min after injection. This increase was prevented by pretreatment with the Y1 receptor antagonist BIBP3226. Immunohistochemistry showed that CRH-immunoreactive neurons coexpressed Y1 receptor immunoreactivity (Y1r-ir) in the PVN, and a majority of these neurons (88.8%) were neuroendocrine as determined by ip injections of FluoroGold. Bilateral infusion of the Y1/Y5 agonist, [leu31pro34]NPY (110 pmol), into the PVN increased c-Fos and phosphorylated cAMP response element-binding protein expression and elevated plasma corticosterone levels. Increased expression of c-Fos and phosphorylated cAMP response element-binding protein was observed in populations of CRH/Y1r-ir cells. The current findings present a comprehensive study of NPY Y1 receptor distribution and activation with respect to CRH neurons in the PVN. The expression of NPY Y1r-ir by neuroendocrine CRH cells suggests that alterations in NPY release and subsequent activation of NPY Y1 receptors plays an important role in the regulation of the HPA.

Bacterial Translocation to Mesenteric Lymph Nodes Increases in Chronic Portal Hypertensive Rats

2009 ◽  
Vol 55 (8) ◽  
pp. 2244-2254 ◽  
Author(s):  
Miguel-Ángel Llamas ◽  
María-Ángeles Aller ◽  
Domingo Marquina ◽  
María-Paz Nava ◽  
Jaime Arias
Keyword(s):  
Lymph Nodes ◽  
Bacterial Translocation ◽  
Hypertensive Rats ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph

scholarly journals Inflammatory Pain and Corticosterone Response in Infant Rats: Effect of 5-HT1A Agonist Buspirone Prior to Gestational Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Irina P. Butkevich ◽  
Viktor A. Mikhailenko ◽  
Tat'yana R. Bagaeva ◽  
Elena A. Vershinina ◽  
Anna Maria Aloisi ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Inflammatory Pain ◽  
Formalin Test ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Plasma Corticosterone Level ◽  
Infant Rats ◽  
Corticosterone Response ◽  
Gestational Stress

Our researches have shown that gestational stress causes exacerbation of inflammatory pain in the offspring; the maternal 5-HT1A agonist buspirone before the stress prevents the adverse effect. The serotonergic system and hypothalamo-pituitary-adrenal (HPA) axis are closely interrelated. However, interrelations between inflammatory pain and the HPA axis during the hyporeactive period of the latter have not been studied. The present research demonstrates that formalin-induced pain causes a gradual and prolonged increase in plasma corticosterone level in 7-day-old male rats; twenty-four hours after injection of formalin, the basal corticosterone level still exceeds the initial basal corticosterone value. Chronic treatments of rat dams with buspirone before restraint stress during gestation normalize in the offspring pain-like behavior and induce during the acute phase in the formalin test the stronger corticosterone increase as compared to the stress hormonal elevation in animals with other prenatal treatments. Negative correlation between plasma corticosterone level and the number of flexes+shakes is revealed in buspirone+stress rats. The new data enhance the idea about relativity of the HPA axis hyporeactive period and suggest that maternal buspirone prior to stress during gestation may enhance an adaptive mechanism of the inflammatory nociceptive system in the infant male offspring through activation of the HPA axis peripheral link.

scholarly journals Vitamin A regulates hypothalamic–pituitary–adrenal axis status in LOU/C rats

2013 ◽  
Vol 219 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Nathalie Marissal-Arvy ◽  
Rachel Hamiani ◽  
Emmanuel Richard ◽  
Marie-Pierre Moisan ◽  
Véronique Pallet
Keyword(s):  
Vitamin A ◽  
Hpa Axis ◽  
Restraint Stress ◽  
Vitamin A Deficiency ◽  
Plasma Corticosterone ◽  
Hypothalamic Pituitary Adrenal ◽  
Corticosteroid Receptors ◽  
Vitamin A Status ◽  
Corticosterone Response ◽  
Hpa Axis Activity

The aim of this study was to explore the involvement of retinoids in the hypoactivity and hyporeactivity to stress of the hypothalamic–pituitary–adrenal (HPA) axis in LOU/C rats. We measured the effects of vitamin A deficiency administered or not with retinoic acid (RA) on plasma corticosterone in standard conditions and in response to restraint stress and on hypothalamic and hippocampal expression of corticosteroid receptors, corticotropin-releasing hormone and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in LOU/C rats. Interestingly, under control conditions, we measured a higher plasma concentration of retinol in LOU/C than in Wistar rats, which could contribute to the lower basal activity of the HPA axis in LOU/C rats. Vitamin A deficiency induced an increased HPA axis activity in LOU/C rats, normalized by RA administration. Compared with LOU/C control rats, vitamin A-deficient rats showed a delayed and heightened corticosterone response to restraint stress. The expression of corticosteroid receptors was strongly decreased by vitamin A deficiency in the hippocampus, which could contribute to a less efficient feedback by corticosterone on HPA axis tone. The expression of 11β-HSD1 was increased by vitamin A deficiency in the hypothalamus (+62.5%) as in the hippocampus (+104.7%), which could lead to a higher production of corticosterone locally and contribute to alteration of the hippocampus. RA supplementation treatment restored corticosterone concentrations and 11β-HSD1 expression to control levels. The high vitamin A status of LOU/C rats could contribute to their low HPA axis activity/reactivity and to a protective effect against 11β-HSD1-mediated deleterious action on cognitive performances during ageing.

scholarly journals A Possible Mechanism for the Action of Adrenomedullin in Brain to Stimulate Stress Hormone Secretion

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 4890-4896 ◽  
Author(s):  
Meghan M. Taylor ◽  
Willis K. Samson
Keyword(s):  
Hpa Axis ◽  
Hormone Secretion ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Stress Hormone ◽  
Elevated Plasma ◽  
The Central Nervous System ◽  
Neuroendocrine Responses ◽  
The Brain

Abstract Adrenomedullin (AM) has been reported to have actions at each level of the hypothalamo-pituitary-adrenal (HPA) axis, suggesting that the peptide plays a role in the organization of the neuroendocrine responses to stress. We examined the mechanism by which AM regulates the central nervous system branch of the HPA axis as well as the possible role of AM in the modulation of the releases of two other hormones, prolactin and GH, whose secretions also are altered by stress. Intracerebroventricular administration of AM led to elevated plasma corticosterone levels in unrestrained, conscious male rats. This effect was abrogated by pretreatment with a CRH antagonist, suggesting that AM activates the HPA axis by causing the release of CRH into hypophyseal portal vessels. In addition, AM given intracerebroventricularly stimulated the release of prolactin but did not alter the secretion of GH. We propose that AM produced in the brain may be an important neuromodulator of the hormonal stress response.

scholarly journals Role of the High Affinity Immunoglobulin E Receptor in Bacterial Translocation and Intestinal Inflammation

2000 ◽  
Vol 193 (1) ◽  
pp. 25-34 ◽  
Author(s):  
David Dombrowicz ◽  
Sophie Nutten ◽  
Pierre Desreumaux ◽  
Christel Neut ◽  
Gérard Torpier ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Bacterial Translocation ◽  
Intestinal Inflammation ◽  
Immunoglobulin E ◽  
Interleukin 4 ◽  
Mesenteric Lymph Nodes ◽  
Bacterial Pathogenicity ◽  
High Affinity ◽  
High Affinity Receptor ◽  
A Cell

A role for immunoglobulin E and its high affinity receptor (FcεRI) in the control of bacterial pathogenicity and intestinal inflammation has been suggested, but relevant animal models are lacking. Here we compare transgenic mice expressing a humanized FcεRI (hFcεRI), with a cell distribution similar to that in humans, to FcεRI-deficient animals. In hFcεRI transgenic mice, levels of colonic interleukin 4 were higher, the composition of fecal flora was greatly modified, and bacterial translocation towards mesenteric lymph nodes was increased. In hFcεRI transgenic mice, 2,4,6-tri-nitrobenzenesulfonic acid (TNBS)-induced colitis was also more pronounced, whereas FcεRI-deficient animals were protected from colitis, demonstrating that FcεRI can affect the onset of intestinal inflammation.

scholarly journals Translocation of 99mTc labelled bacteria after intestinal ischemia and reperfusion

2004 ◽  
Vol 19 (4) ◽  
pp. 328-333 ◽  
Author(s):  
Samir Assi João ◽  
Suelene Suassuna Silvestre de Alencar ◽  
Aldo da Cunha Medeiros ◽  
Simone Otília Fernandes Diniz ◽  
Valbert Nascimento Cardoso ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Intestinal Ischemia ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph ◽  
Colony Forming Units ◽  
Male Wistar Rats ◽  
Intestinal Ischemia Reperfusion

PURPOSE: Ischemia and reperfusion of the small intestine disrupts gut barrier, causes bacterial translocation and activates inflammatory responses. An experimental study was planned to evaluate if 99mTc labelled Escherichia coli translocates to mesenteric lymph nodes, liver, spleen, lung and serum of rats submitted to mesenteric ischemia/reperfusion. Additionally, it was observed if the time of reperfusion influences the level of translocation. METHODS: Forty male Wistar rats underwent 45 minutes of gut ischemia by occlusion of the superior mesenteric artery. The translocation of labelled bacteria to different organs and portal serum was determined in rats reperfused for 30 minutes, 24 hours, sham(S) and controls(C), using radioactivity count and colony forming units/g (CFU). RESULTS: All the organs from rats observed for 24 hours after reperfusion had higher levels of radioactivity and positive cultures (CFU) than did the organs of rats reperfused for 30 minutes, C and S, except in the spleen (p<0,01). CONCLUSION: The results of this study indicated that intestinal ischemia/reperfusion led to bacterial translocation, mostly after 24 hours of reperfusion.

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