scholarly journals Hypothalamic neurochemical changes in long-term recovered bilateral subdiaphragmatic vagotomized rats

Author(s):  
Anna Teresa Kobrzycka ◽  
Adrian Mateusz Stankiewicz ◽  
Joanna Goscik ◽  
Monika Gora ◽  
Beata Burzynska ◽  
...  

Abstract BackgroundVagus nerve is one of the crucial routes in communication between immune and central nervous systems. Impaired vagal nerve function may intensify peripheral inflammatory processes. This effect subsides along with prolonged recovery after permanent nerve injury. One of the results of such compensation is a normalized plasma concentration of stress hormone corticosterone – a marker of hypothalamic-pituitary-adrenal (HPA) axis activity. In the present work we strive to explain this corticosterone normalization by studying the mechanisms responsible for compensation-related neurochemical alterations in the hypothalamus. Methods Using microarrays and HPLC we measured genome-wide gene expression and major amino acid neurotransmitters content in hypothalamus of bilaterally vagotomized rats, one month after surgery.ResultsOur results show that, in the long-term, vagotomy affects hypothalamic amino acids concentration but not mRNA expression of tested genes.ConclusionsWe propose an alternative pathway of immune to CNS communication after vagotomy, leading to activation of HPA axis, by influencing central amino acids and subsequent monoaminergic neurotransmission.

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S259
Author(s):  
Santosh Kumar Prajapati ◽  
Sairam Krishnamurthy

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Elizabeth Asztalos

Preterm birth remains a major health issue worldwide. Since the 1990s, women at risk for preterm birth received a single course of exogenous antenatal corticosteroids (ACSs) to facilitate fetal lung maturity. More recently, repeated or multiple courses of ACS have been supported to provide continued fetal maturity support for women with continued risk of preterm birth. However, exogenous ACS reduces birth weight which, in turn, is associated with adverse adult outcomes such as coronary heart disease, stroke, hypertension, and type 2 diabetes. The long-term effects of ACS exposure on HPA axis activity and neurological function are well documented in animal studies, and it appears that ACS, regardless of dose exposure, is capable of affecting fetal HPA axis development causing permanent changes in the HPA axis that persists through life and is manifested by chronic illness and behavioral changes. The challenge in human studies is to demonstrate whether an intervention such as ACS administration in pregnancy contributes to developmental programming and how this is manifested in later life.


Endocrinology ◽  
2009 ◽  
Vol 150 (6) ◽  
pp. 2709-2716 ◽  
Author(s):  
Mathias V. Schmidt ◽  
Vera Sterlemann ◽  
Klaus Wagner ◽  
Bertram Niederleitner ◽  
Karin Ganea ◽  
...  

A tight regulation of hypothalamic-pituitary-adrenal (HPA) axis activity is essential for successful adaptation to stressful stimuli. Disruption of normal HPA axis development is a main risk factor for diseases such as posttraumatic stress disorder or depression, but the molecular mechanisms that lead to these long-term consequences are poorly understood. Here, we test the hypothesis that the pituitary glucocorticoid receptor (GR) is involved in regulating HPA axis function in neonatal and adult animals. Furthermore, we investigate whether postnatal hypercortisolism induced by pituitary GR deficiency is a main factor contributing to the persistent effects of early-life stress. Conditional knockout mice with a deletion of the GR at the pituitary (GRPOMCCre) show excessive basal corticosterone levels during postnatal development, but not in adulthood. The hypercortisolemic state of neonatal GRPOMCCre mice is accompanied by central gene expression changes of CRH and vasopressin in the paraventricular nucleus, but these alterations normalize at later ages. In adult mice, pituitary GR deficiency results in impaired glucocorticoid negative feedback. Furthermore, adult GRPOMCCre mice display a more active coping strategy in the forced swim test, with no alterations in anxiety like behavior or cognitive functions. Postnatal GR antagonist treatment is able to prevent the long-term behavioral effects in GRPOMCCre mice. In conclusion, we show that pituitary GRs are centrally involved in regulating HPA axis activity in neonates and mediate negative feedback regulation in adult animals. Postnatal glucocorticoid excess results in an altered stress-coping behavior in adult animals, with no effects on anxiety like behavior or cognition.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Wenxiao Du ◽  
Xiaoli Chen ◽  
Min Shi ◽  
Fuhua Bian ◽  
Zhenjun Zhao

AbstractRecent studies have shown that long-term alcohol intake from food can lead to numerous mental disorders in humans, and the social and health effects of excessive intake of alcohol currently represent serious problems for governments and families worldwide. However, to date, it has not been determined how alcohol affects the hypothalamic–pituitary–adrenal (HPA) axis. The zebrafish offers a good model for studying the toxicology of food-grade ethanol. In the present study, using zebrafish larvae exposed to 1% ethanol, we performed zebrafish behavioral analysis. Samples were collected for enzyme-linked immunosorbent assay (ELISA) and quantitative real time-polymerase chain reaction (qRT-PCR) experiments, and statistical analysis was performed. We found that ethanol decreased the locomotor activity of zebrafish larvae, which showed a more intense reaction to external stimuli. Ethanol also increased the level of HPA axis hormones in zebrafish larvae, influenced the level of neurotransmitters, and altered the expression of key genes in neurotransmitter metabolism. Ethanol exposure affects zebrafish behavior, increases the level of HPA axis hormones in zebrafish larvae, affects the level of neurotransmitters, and affects the expression of key genes in dopamine and serotonin metabolism. These findings may help to elucidate the effects of ethanol on HPA axis activity.


2019 ◽  
Vol 105 (3) ◽  
pp. e575-e582
Author(s):  
Liesa Ilg ◽  
Clemens Kirschbaum ◽  
Shu-Chen Li ◽  
Pauline Wimberger ◽  
Katharina Nitzsche ◽  
...  

Abstract Context Antenatal synthetic glucocorticoid (sGC) treatment constitutes a potent programming factor of the hypothalamic–pituitary–adrenal (HPA) axis. Previous findings from our group revealed long-term changes in cortisol stress reactivity following antenatal sGC therapy. However, the few prior studies exclusively relied on spot measurements of phasic HPA axis activity, which may not adequately capture cortisol output over prolonged periods of time. Objective To address this gap, the current study utilized hair steroid concentrations, a valid marker of integrated long-term HPA-axis activity, to investigate endocrine changes in individuals treated with antenatal sGC. Design, Setting, and Participants This cross-sectional study comprised 76 term-born children (7–12 years) and 58 adolescents (14–18 years). Cumulated hormonal secretion in scalp hair over a 3-month period was determined for different biomarkers of tonic HPA axis activity by liquid chromatography coupled with tandem mass spectrometry. Hair steroid levels were compared between participants with antenatal sGC therapy (dexamethasone or betamethasone) and different control groups. Results Findings from this study provide no evidence for a significant effect of antenatal sGCs on long-term hair steroid concentrations. Participants treated with antenatal sGC exhibited comparable levels of hair cortisol, cortisone, dehydroepiandrosterone, and cortisol/dehydroepiandrosterone ratios compared to those of mothers who had been admitted to hospital for pregnancy complications but had never received sGC therapy and controls from physiological pregnancies. Conclusion In conjunction with data from previous studies, it is thus tempting to speculate that sGC may affect the capacity of dynamic changes and flexible adaption of an individual’s HPA axis rather than changes in tonic steroid output.


2020 ◽  
Author(s):  
wenxiao du ◽  
Xiaoli Chen ◽  
Zhenjun Zhao ◽  
min shi ◽  
fuhua bian

Abstract Long-term alcohol intake from food can lead to numerous mental disorders in humans, and cause serious problems for governments and families worldwide. However, currently, it is unclear how alcohol affects the hypothalamic–pituitary–adrenal (HPA) axis. In the present study, using zebrafish larvae exposed to 1% ethanol, we made Zebrafish behavioural analysis, samples were collected for the enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) experiments,and made statistical analyses at last. we found that ethanol decreases the locomotor activity of zebrafish larvae,showed a more intense reaction to external stimuli,increases the secretion of HPA axis hormones in zebrafish larvae,influences the secretion of neurotransmitters,alters key gene expression during neurotransmitter metabolism. Ethanol exposure reduced zebrafish locomotor activity, increased their HPA axis activity, and led to significant changes in the secretion of dopamine and serotonin. These findings provide us with a new understanding of the effects of ethanol on the HPA axis.


2010 ◽  
Vol 22 (1) ◽  
pp. 165-175 ◽  
Author(s):  
Penelope K. Trickett ◽  
Jennie G. Noll ◽  
Elizabeth J. Susman ◽  
Chad E. Shenk ◽  
Frank W. Putnam

AbstractInconsistencies exist in literature examining hypothalamic–pituitary–adrenal (HPA) axis activity in children and adults who have experienced childhood abuse. Hence, the extent and manner to which childhood abuse may disrupt HPA axis development is largely unknown. To address these inconsistencies, the developmental course of nonstress cortisol in a long-term longitudinal study was assessed at six time points from childhood through adolescence and into young adulthood to determine whether childhood abuse results in disrupted cortisol activity. Nonstress, morning cortisol was measured in 84 females with confirmed familial sexual abuse and 89 nonabused, comparison females. Although dynamically controlling for co-occurring depression and anxiety, hierarchical linear modeling (HLM) showed that relative to comparison females, the linear trend for abused females was significantly less steep when cortisol was examined across development from age 6 to age 30,t(1, 180) = −2.55,p< .01, indicating attenuation in cortisol activity starting in adolescence with significantly lower levels of cortisol by early adulthood,F(1, 162) = 4.78,p< .01. As a more direct test of the attenuation hypothesis, supplemental HLM analyses of data arrayed by time since the disclosure of abuse indicated that cortisol activity was initially significantly higher,t(1, 425) = 2.18,p< .05, and slopes were significantly less steept(1, 205) = −2.66,p <.01, for abused females. These findings demonstrate how the experience of childhood abuse might disrupt the neurobiology of stress, providing some support for the attenuation hypothesis that victims of abuse may experience cortisol hyposecretion subsequent to a period of heightened secretion.


2020 ◽  
Vol 23 (1) ◽  
pp. 33-38 ◽  
Author(s):  
Britt J. van Keulen ◽  
Conor V. Dolan ◽  
Ruth Andrew ◽  
Brian R. Walker ◽  
Hilleke E. Hulshoff Pol ◽  
...  

AbstractLife-course experiences have been postulated to program hypothalamus–pituitary–adrenal (HPA) axis activity, suggesting that HPA axis activity is, at least partially, stable over time. Yet, there is paucity of data on the long-term stability of cortisol production and metabolism. We performed a prospective follow-up study in twins recruited from a nationwide register to estimate the stability of cortisol production and metabolism over time, and the contribution of genetic and environmental factors to this stability. In total, 218 healthy mono- and dizygotic twins were included. At the ages of 9, 12 and 17 years, morning urine samples were collected for assessment (by gas chromatography-tandem mass spectrometry) of cortisol metabolites, enabling the calculation of cortisol metabolite excretion rate and cortisol metabolism activity. Our results showed a low stability for both cortisol metabolite excretion rate (with correlations <.20) and cortisol metabolism activity indices (with correlations of .25 to .46 between 9 and 12 years, −.02 to .15 between 12 and 17 years and .09 to .28 between 9 and 17 years). Because of the low stability over time, genetic and environmental contributions to this stability were difficult to assess, although it seemed to be mostly determined by genetic factors. The low stability in both cortisol production and metabolism between ages 9 and 17 years reflects the dynamic nature of the HPA axis.


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