scholarly journals Divergent Roles of the CRH Receptors in the Control of Gonadotropin Secretion Induced by Acute Restraint Stress at Proestrus

Endocrinology ◽  
2012 ◽  
Vol 153 (10) ◽  
pp. 4838-4848 ◽  
Author(s):  
Guillermo A. Ariza Traslaviña ◽  
Celso Rodrigues Franci
Keyword(s):  
Restraint Stress ◽  
Acute Stress ◽  
Reproductive Function ◽  
Brain Regions ◽  
Noradrenergic Neurons ◽  
Gonadotropin Secretion ◽  
Acute Restraint Stress ◽  
Lh Secretion ◽  
Crh Receptors ◽  
Stimulation Of

Abstract CRH has been implicated as a mediator of stress-induced effects on the hypothalamus-pituitary-gonad axis, acting via CRH receptors in various brain regions. We investigated whether the effects of restraint stress on the secretion of gonadotropins on the morning of proestrus are mediated by the CRH-R1 or CRH-R2 receptors in the oval subdivision of the anterolateral BST, the central amygdala, the locus coeruleus (LC), or the A1 and A2 neuron groups in the medulla. At proestrus morning, rats were injected with antalarmin (a CRH-R1 antagonist), asstressin2-B (a CRH-R2 antagonist) or vehicles. Thirty minutes after the injection, the animals were placed into restraints for 30 min, and blood was sampled for 2 h. At the end of the experiment, the brains were removed for immunofluorescence analyses. Restraint stress increased the levels of FSH and LH. Antalarmin blocked the stress-induced increases in FSH and LH secretion, but astressin2-B only blocked the increase in FSH secretion. LC showed intense stress-induced neuronal activity. FOS/tyrosine-hydroxylase coexpression in LC was reduced by antalarmin, but not astressin2-B. The CRH-R1 receptor, more than CRH-R2 receptor, appears to be essential for the stimulation of the hypothalamus-pituitary-gonad axis by acute stress; this response is likely mediated in part by noradrenergic neurons in the LC. We postulate that the stress-induced facilitation of reproductive function is mediated, at least in part, by CRH action through CRH-R1 on noradrenaline neurons residing in the LC that trigger GnRH discharge and gonadotropin secretion.

scholarly journals Maintenance of Gonadotropin Secretion by Glucocorticoids under Stress Conditions through the Inhibition of Prostaglandin Synthesis in the Brain

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1087-1093 ◽  
Author(s):  
Takashi Matsuwaki ◽  
Yuko Kayasuga ◽  
Keitaro Yamanouchi ◽  
Masugi Nishihara
Keyword(s):  
Restraint Stress ◽  
Acute Stress ◽  
Reproductive Function ◽  
Stress Conditions ◽  
Ovariectomized Rats ◽  
Gonadotropin Secretion ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Corticosterone Treatment ◽  
Factor Α ◽  
The Brain

We have previously reported that glucocorticoids counteract the suppressive effects of tumor necrosis factor-α on both pulsatile and surge secretion of LH. This suggests that glucocorticoids have a protective effect on reproductive function under infectious stress. In the present study, we examined whether glucocorticoids maintain pulsatile LH secretion under various conditions of acute stress and the possible involvement of prostaglandins (PGs) in glucocorticoid actions. Three different types of stressors, namely infectious (lipopolysaccharide, 0.5 μg/kg), hypoglycemic (2-deoxy-d-glucose, 100 mg/kg), and restraint stress (1 h) were applied to ovariectomized rats. In ovariectomized rats, LH pulses were partially suppressed by restraint, but not by lipopolysaccharide or 2-deoxy-d-glucose. On the other hand, adrenalectomy (ADX) significantly enhanced the suppressive effects of all the stressors applied on LH pulses. Treatment with both corticosterone (25 mg/kg) and indomethacin (10 mg/kg) in ADX rats significantly attenuated the suppressive effects of these stressors on LH pulses. In addition, the immunoreactivity of cyclooxygenase-2, a PG-synthesizing enzyme, in the brain under stress conditions was much enhanced by ADX, and this was counteracted by corticosterone treatment. Similarly, an increase in body temperature under restraint stress was enhanced by ADX and suppressed by corticosterone. These results suggest that suppression of LH pulsatility by stress is mediated by PGs in the brain, and that increased release of endogenous glucocorticoids in response to stress counteracts this suppression by inhibiting PG synthesis, and thereby maintains reproductive function regardless of the nature of the stressor.

scholarly journals Corticotropin-Releasing Hormone and Its Structurally Related Urocortin Are Synthesized and Secreted by Human Mast Cells

Endocrinology ◽  
2004 ◽  
Vol 145 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Duraisamy Kempuraj ◽  
Nikoletta G. Papadopoulou ◽  
Michael Lytinas ◽  
Man Huang ◽  
Kristiana Kandere-Grzybowska ◽  
...  
Keyword(s):  
Mast Cells ◽  
Immune Responses ◽  
Restraint Stress ◽  
Acute Stress ◽  
Rt Pcr ◽  
Human Cord Blood ◽  
Potential Source ◽  
First Time ◽  
Pituitary Adrenal Axis ◽  
Stimulation Of

Abstract Stress activates the hypothalamic-pituitary-adrenal axis through CRH, leading to production of glucocorticoids that down-regulate immune responses. However, acute stress also has proinflammatory effects. We previously showed that restraint stress, as well as CRH and its structurally related urocortin (Ucn), could activate mast cells and trigger mast cell-dependent vascular permeability. Here we show for the first time that human cord blood-derived cultured mast cells (hCBMC) at 10 wk, but not at 2 wk, are immunocytochemically positive for CRH and Ucn; human leukemic mast cells are weakly positive for both peptides. The ability of these mast cells to synthesize CRH and Ucn was confirmed by showing mRNA expression with RT-PCR. hCBMC (8–14 wk) synthesize and store 1–10 ng/106 cells (10–20 μg/g) of both CRH and Ucn detected by ELISA of cell homogenates. Stimulation of IgE-sensitized hCBMC with anti-IgE results in secretion of most CRH and Ucn. These findings indicate that mast cells are not only the target, but also a potential source of CRH and Ucn that could have both autocrine and paracrine functions, especially in allergic inflammatory disorders exacerbated by stress.

scholarly journals Direct stimulatory effect of ghrelin on pituitary release of LH through a nitric oxide-dependent mechanism that is modulated by estrogen

Reproduction ◽  
2007 ◽  
Vol 133 (6) ◽  
pp. 1223-1232 ◽  
Author(s):  
Rafael Fernández-Fernández ◽  
Manuel Tena-Sempere ◽  
Juan Roa ◽  
Juan Manuel Castellano ◽  
Víctor M Navarro ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reproductive Function ◽  
Female Rats ◽  
Experimental Conditions ◽  
Gonadotropin Secretion ◽  
Minimal Effective Dose ◽  
Gh Secretion ◽  
Lh Secretion

Ghrelin, a gut peptide with key actions on food intake and GH secretion, has been recently recognized as potential regulator of reproductive function. Thus, in adult female rats, ghrelin has been proven to modulate GnRH/LH secretion, with predominant inhibitory effectsin vivo. We analyze herein potential direct pituitary effects of ghrelin on basal and GnRH-stimulated gonadotropin secretion in prepubertal female rats, and its interplay with ovarian inputs, nitric oxide (NO), and hypothalamic differentiation. In the experimental setting, pituitaries from intact and ovariectomized prepubertal female rats were challenged with ghrelinin vitroand LH secretion was monitored. Our results demonstrate that 1) ghrelin consistently stimulatedin vitropituitary LH secretion under different experimental conditions; 2) the sensitivity to ghrelin, expressed either as the minimal effective dose or the amplitude of the LH response, was modulated by ovarian inputs; 3) the blockade of estrogen action significantly augmented the stimulatory effect of ghrelin; 4) the stimulatory effect of ghrelin on LH secretion required proper NO synthesis; and 5) the ability of ghrelin to elicit LH secretionin vitrowas preserved after alteration (masculinization) of brain sexual differentiation. Overall, our present data reinforce the concept that ghrelin participates in the control of LH secretion, with potential stimulatory actions at the pituitary level that require the presence of NO and are modulated by ovarian signals.

scholarly journals Temporal expression of estrogen receptor α in the hypothalamus and medulla oblongata during fasting: a role of noradrenergic neurons

2006 ◽  
Vol 190 (3) ◽  
pp. 593-600 ◽  
Author(s):  
Beverly A S Reyes ◽  
Hiroko Tsukamura ◽  
Helen I’Anson ◽  
Maria Amelita C Estacio ◽  
Kanjun Hirunagi ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Brain Regions ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Noradrenergic Neurons ◽  
Anatomical Relationship ◽  
Relationship Of ◽  
Lh Secretion

Fasting-induced LH suppression is augmented by estrogen in female rats. We investigated the temporal changes in the number of estrogen receptor α (ERα)-immunoreactive (ir) cells in various brain regions in ovariectomized rats fasted for 6, 24, 30, and 48 h, commencing at 1300 h. We also determined the anatomical relationship of ERα immunoreactivity and dopamine-β-hydroxylase (DBH) neurons in the A2 region of the nucleus of the solitary tract (NTS) and the paraventricular nucleus (PVN). The number of ERα-ir cells significantly increased after 30 h from the onset of fasting in the PVN and NTS compared with the unfasted controls and was sustained until 48 h. In the A2 region of 48-h fasted rats, 46.75% DBH-ir cells expressed ERα, and this was significantly higher than in unfasted controls (8.16% DBH-ir cells expressed ERα). In the PVN, most ERα-ir neurons were juxtaposed with DBH-ir varicosities. These results suggest that ERα is expressed in specific brain regions at a defined time from the onset of fasting. In addition, the anatomical relationship of noradrenergic and ERα-ir neurons in the A2 region and PVN may suggest a role for estrogen in increasing the activity of noradrenergic neurons in the A2 region and enhancing sensitivity of the PVN to noradrenergic input arising from the lower brainstem and thereby augmenting the suppression of LH secretion during fasting.

scholarly journals Putative Activation of the CB1 Cannabinoid Receptors Prevents Anxiety-Like Behavior, Oxidative Stress, and GABA Decrease in the Brain of Zebrafish Submitted to Acute Restraint Stress

2021 ◽  
Vol 14 ◽  
Author(s):  
Waldo Lucas Luz ◽  
Mateus Santos-Silva ◽  
Patrick Bruno Cardoso ◽  
Nadyme Assad ◽  
Edinaldo Rogério da Silva Moraes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Restraint Stress ◽  
Cannabinoid Receptors ◽  
Acute Stress ◽  
Control Treatment ◽  
Cb1 Receptors ◽  
Acute Restraint Stress ◽  
Gaba Content ◽  
The Brain

Anxiety disorder is a well-recognized condition observed in subjects submitted to acute stress. Although the brain mechanisms underlying this disorder remain unclear, the available evidence indicates that oxidative stress and GABAergic dysfunction mediate the generation of stress-induced anxiety. Cannabinoids are known to be efficient modulators of behavior, given that the activation of the cannabinoid receptors type-1 (CB1 receptors) induces anxiolytic-like effects in animal models. In the present study, we aimed to describe the effects of the stimulation of the CB1 receptors on anxiety-like behavior, oxidative stress, and the GABA content of the brains of zebrafish submitted to acute restraint stress (ARS). The animals submitted to the ARS protocol presented evident anxiety-like behavior with increased lipid peroxidation in the brain tissue. The evaluation of the levels of GABA in the zebrafish telencephalon presented decreased levels of GABA in the ARS group in comparison with the control. Treatment with ACEA, a specific CB1 receptor agonist, prevented ARS-induced anxiety-like behavior and oxidative stress in the zebrafish brain. ACEA treatment also prevented a decrease in GABA in the telencephalon of the animals submitted to the ARS protocol. Overall, these preclinical data strongly suggest that the CB1 receptors represent a potential target for the development of the treatment of anxiety disorders elicited by acute stress.

scholarly journals Urocortin 3 in the posterodorsal medial amygdala mediates psychosocial stress-induced suppression of LH pulsatility in female mice

2021 ◽  
Author(s):  
Deyana Ivanova ◽  
Xiao-Feng Li ◽  
Caitlin McIntyre ◽  
Yali Liu ◽  
Lingsi Kong ◽  
...  
Keyword(s):  
Psychosocial Stress ◽  
Restraint Stress ◽  
Pulse Generator ◽  
Reproductive Function ◽  
Suppressive Effect ◽  
Medial Amygdala ◽  
Reproductive Axis ◽  
Lh Pulsatility ◽  
As Stress ◽  
Lh Secretion

Exposure to psychosocial stress disrupts reproductive function and interferes with pulsatile luteinising hormone (LH) secretion in mammals. The posterodorsal sub-nucleus of the medial amygdala (MePD) is part of the limbic brain and is an upstream modulator of the reproductive axis as well as stress and anxiety states. Corticotropin releasing factor type-2 receptors (CRFR2) are activated in the presence of psychosocial stress together with an increased expression of the CRFR2 ligand Urocortin3 (Ucn3) in MePD of rodents. We investigate whether Ucn3 signalling in the MePD is involved in mediating the suppressive effect of psychosocial stress exposure on LH pulsatility. Firstly, we administered Ucn3 into the MePD and monitored the effect on pulsatile LH secretion in ovariectomised mice. Next, we delivered Astressin2B, a highly selective CRFR2 antagonist, intra-MePD in the presence of predator odor, 2,4,5-Trimethylthiazole (TMT) and examined the effect on LH pulses. Subsequently, we virally infected ovariectomised Ucn3-cre-tdTomato mice with inhibitory DREADDs targeting the MePD Ucn3 neurons while exposing the mice to TMT or restraint stress and examined the effect on LH pulsatility as well as corticosterone (CORT) release. Administration of Ucn3 into the MePD dose-dependently inhibited pulsatile LH secretion and intra-MePD administration of Astressin2B blocked the suppressive effect TMT on LH pulsatility. Additionally, DREADDs inhibition of MePD Ucn3 neurons blocked TMT and restraint stress-induced inhibition of LH pulses as well as CORT release in the presence of TMT. These results demonstrate for the first time that Ucn3 neurons in the MePD mediate psychosocial stress-induced suppression of the GnRH pulse generator and psychosocial stress-induced CORT secretion. Ucn3 signalling in the MePD plays a fundamental role in modulating the hypothalamic-pituitary-ganadal and hypothalamic-pituitary-adrenal axes, and this brain locus may represent a nodal centre in the crosstalk between the reproductive and stress axes.

Nerve Injury Alters Restraint-induced Activation of the Basolateral Amygdala in Male Rats

2021 ◽  
Author(s):  
James Kang ◽  
David Mor ◽  
Kevin A Keay
Keyword(s):  
Prefrontal Cortex ◽  
Nerve Injury ◽  
Restraint Stress ◽  
Basolateral Amygdala ◽  
Acute Stress ◽  
Male Rats ◽  
Neuronal Activation ◽  
Acute Restraint Stress ◽  
The Right ◽  
Psychological Stressor

Abstract The amygdala is critical for the production of appropriate responses towards emotional or stressful stimuli. It has a characteristic neuronal activation pattern to acute stressors. Chronic pain and acute stress have each been shown to independently modulate the activity of the amygdala. Few studies have investigated the effect of pain or injury, on amygdala activation to acute stress. This study investigated the effects of a neuropathic injury on the activation response of the amygdala to an acute restraint stress. Chronic constriction injury of the right sciatic nerve (CCI) was used to create neuropathic injury and a single brief 15-minute acute restraint was used as an emotional/psychological stressor. All rats received cholera toxin B (CTB) retrograde tracer injections into the medial prefrontal cortex (mPFC) to assess if the amygdala to mPFC pathway was specifically regulated by the combination of neuropathic injury and acute stress. To assess differential patterns of activity in amygdala subregions, cFos expression was used as a marker for “acute”, restraint triggered neuronal activation, and FosB/DFosB expression was used to reveal prolonged neuronal activation / sensitisation triggered by CCI. Restraint resulted in a characteristic increase in cFos expression in the medial amygdala, which was not altered by CCI. Rats with a CCI showed increased cFos expression in the basolateral amygdala (BLA), in response to an acute restraint stress, but not in neurons projecting to the prefrontal cortex. Further, CCI rats showed an increase in FosB/ΔFosB expression which was exclusive to the BLA. This increase likely reflects sensitisation of the BLA as a consequence of nerve injury which may contribute to heightened sensitivity of BLA neurons to acute emotional/ psychological stressors.

scholarly journals Brain Region Specific Monoamine and Oxidative Changes During Restraint Stress

2012 ◽  
Vol 39 (3) ◽  
pp. 311-318 ◽  
Author(s):  
Ausaf Ahmad ◽  
Naila Rasheed ◽  
Ghulam Md Ashraf ◽  
Rajnish Kumar ◽  
Naheed Banu ◽  
...  
Keyword(s):  
Frontal Cortex ◽  
Stress Responses ◽  
Restraint Stress ◽  
Acute Stress ◽  
Initial Response ◽  
Brain Regions ◽  
Antioxidant Systems ◽  
Time Intervals ◽  
Oxidative Processes ◽  
Selective Increase

Background and Purpose:Stress-induced central effects are regulated by brain neurotransmitters, glucocorticoids and oxidative processes. Therefore, we aimed to evaluate the simultaneous alterations in the monoamine and antioxidant systems in selected brain regions (frontal cortex, striatum and hippocampus) at 1 hour (h) and 24h following the exposure of restraint stress (RS), to understand their initial response and possible crosstalk.Methods and Results:RS (150 min immobilization) significantly increased the dopamine levels in the frontal cortex and decreased them in the striatum and hippocampus, with selective increase of dopamine metabolites both in the 1h and 24h RS groups compared to control values. The serotonin and its metabolite levels were significantly increased in both time intervals, while noradrenaline levels were decreased in the frontal cortex and striatum only. The activities of superoxide dismutase, glutathione peroxidase and the levels of lipid peroxidation were significantly increased with significant decrease of glutathione levels in the frontal cortex and striatum both in the 1h and 24h RS groups. There was no significant change in the catalase activity in any group. In the hippocampus, the glutathione levels were significantly decreased only in the 1h RS group.Conclusions:Our study implies that the frontal cortex and striatum are more sensitive to oxidative burden which could be related to the parallel monoamine perturbations. This provides a rational look into the simultaneous compensatory central mechanisms operating during acute stress responses which are particular to precise brain regions and may have long lasting effects on various neuropathological alterations.

scholarly journals The vagus nerve is critical for regulation of hypothalamic-pituitary-adrenal axis responses to acute stress

2021 ◽  
Author(s):  
Bailey N Keller ◽  
Angela E Snyder ◽  
Caitlin R Coker ◽  
Elizabeth A Aguilar ◽  
Mary K O'Brien ◽  
...  
Keyword(s):  
Vagus Nerve ◽  
Hpa Axis ◽  
Restraint Stress ◽  
Acute Stress ◽  
Plasma Corticosterone ◽  
Action Potential Firing ◽  
Acute Restraint Stress ◽  
Potential Firing ◽  
Crf Neurons ◽  
Hpa Function

The hypothalamic pituitary adrenal (HPA) axis is a critical regulator of physiologic and psychological responses to acute and chronic stressors. HPA axis function is control by numerous feedback inhibitory mechanisms, disruptions of which can lead to various psychiatric conditions, such as depression, posttraumatic stress disorder, and schizophrenia. Vagus nerve stimulation has been shown to be efficacious in these various mental health issues potentially via modulation of HPA axis function, but the mechanisms by which the vagus nerve may regulate HPA function has not been fully elucidated. In the present studies, we sought to test the hypothesis that the vagus nerve is a critical regulator of HPA function. Neuroendocrine function and neurocircuit changes in corticotropin releasing factor (CRF) neurons in the paraventricular nucleus of the hypothalamus (PVN) was examined following acute stress after subdiaphragmatic left vagotomy (VX) in adult male Sprague-Dawley rats. We found that VX mimics HPA activation seen in sham surgery animals exposed to acute restraint stress, particularly increased plasma corticosterone levels, elevated PVN CRF mRNA, and increased action potential firing of putative CRF neurons in PVN brain slices. Furthermore, VX animals exposed to acute restraint stress showed increased elevations of plasma corticosterone and PVN CRF mRNA which may be due to lack of compensatory PVN GABAergic signaling in response to acute stress. Both Sham/Stress and VX/no stress conditions increases action potential firing in putative PVN CRF neurons, but this effect was not seen in the VX/stress condition, suggesting that not all forms of stress compensation are lost following VX. Overall, these findings suggest that the vagus nerve may play a critical role in regulating HPA axis function via modulation of local PVN neurocircuit activity.

Acute stress in adolescence vs early adulthood following selective deletion of dysbindin-1A: Effects on anxiety, cognition and other schizophrenia-related phenotypes

2019 ◽  
Vol 33 (12) ◽  
pp. 1610-1619 ◽  
Author(s):  
Lieve Desbonnet ◽  
Colm MP O’Tuathaigh ◽  
Clare O’Leary ◽  
Rachel Cox ◽  
Orna Tighe ◽  
...  
Keyword(s):  
Gene Expression ◽  
Object Recognition ◽  
Restraint Stress ◽  
Acute Stress ◽  
Novel Object Recognition ◽  
The Novel ◽  
Object Recognition Test ◽  
Novel Object ◽  
Acute Restraint Stress ◽  
Novel Object Recognition Test

Background: As exposure to stress has been linked to the onset and maintenance of psychotic illness, its pathogenesis may involve environmental stressors interacting with genetic vulnerability. Aim: To establish whether acute stress interacts with a targeted mutation of the gene encoding the neurodevelopmental factor dystrobrevin-binding protein 1 (DTNBP1), resulting in a specific loss of the isoform dysbindin-1A, to influence schizophrenia-relevant phenotypes in mice during adolescence and adulthood. Methods: Male and female mice with a heterozygous or homozygous deletion of DTNBP1 were assessed in the open field test following acute restraint stress in adolescence (Day 35) and young adulthood (Day 60–70). Effects of acute restraint stress on memory retention in the novel object recognition test was also assessed in adulthood. Baseline corticosterone was measured in serum samples and, brain-derived neurotrophic factor (BDNF), glucocorticoid and mineralocorticoid receptor gene expression levels were measured in the hippocampus of adult mice. Results: In the open field, deletion of dysbindin-1A induced hyperactivity and attenuated the action of stress to reduce hyperactivity in adolescence but not in adulthood; in females deletion of dysbindin-1A attenuated the effect of acute stress to increase anxiety-related behaviour in adolescence but not in adulthood. In the novel object recognition test, deletion of dysbindin-1A impaired memory and also revealed an increase in anxiety-related behaviour and a decrease in hippocampal BDNF gene expression in males. Conclusions: These data suggest that deletion of dysbindin-1A influences behaviours related to schizophrenia and anxiety more robustly in adolescence than in adulthood and that dysbindin-1A influences stress-related responses in a sex-dependent manner.

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