Objective To observe the effects of total glucosides of white paeony(GWP) on psychological ethology and neuroendocrine system of stress rats. Methods Ten male Sprague-Dawley rats were treated as normal control group, the others(n=40) were constructed by isolated custody and chronic unpredictable stimuli to build the model of stress rats.Stress rats were randomly divided into 4 groups:model control group,GWP high dose group and low dose(66,33 mg·kg-1) group,fluoxetine(5.0 mg·kg-1) group,each group had 10 rats.The changes of rat behavior were monitored by locomotor activity system.The change of emotion was observed by tail suspension test.The pathology change of adrenal was observed by HE staining.The levels of CorT and ACTH in serum were measured by radioimmunoassay.The expression of CRH mRNA of hypothalamic were detected by RT-PCR. Results The activity of the level scoring and vertical scoring of GWP high dose group was obviously improved as compared to that in model control group,while static time was significantly shortened,Adrenal index of GWP groups were increased significantly(P<0.05) ,thymus index of the treatment group was declined(P<0.05),CorT and ACTH content were decreased (P<0.05) and hypothalamus CRH mRNA of GWP group was decreased(P<0.05) . Conclusion The improvement of activity and related hormone anomalous changes were observed in rats treated with GWP.The mechanism of its actions might be involved adjusting the endocrine function,decreasing CorT and ACTH content and the expression of hypothalamic CRH mRNA of stress rats.
Key words:
Total glucosides of white paeony
;
Hypothalamic-pituitary-adrenal
;
Activity
;
Rats, stress
Fig.1
Pathological images of five groups of rats (HE staining,×20) A.normal control group;B.model control group;C.fluoxetine group ;D.high-dose total glucosides of white paeony (GWP)group ;E.low-dose GWP group
MAGUIREJ,SALPEKAR JA.Stress,seizures,and hypo-thalamic-pituitary-adrenal axis targets for the treatment of epilepsy[J].Epilepsy Behav,2013,26(3):352-362.
Abstract Epilepsy is a heterogeneous condition with varying etiologies including genetics, infection, trauma, vascular, neoplasms, and toxic exposures. The overlap of psychiatric comorbidity adds to the challenge of optimal treatment for people with epilepsy. Seizure episodes themselves may have varying triggers; however, for decades, stress has been commonly and consistently suspected to be a trigger for seizure events. This paper explores the relationship between stress and seizures and reviews clinical data as well as animal studies that increasingly corroborate the impact of stress hormones on neuronal excitability and seizure susceptibility. The basis for enthusiasm for targeting glucocorticoid receptors for the treatment of epilepsy and the mixed results of such treatment efforts are reviewed. In addition, this paper will highlight recent findings identifying a regulatory pathway controlling the body's physiological response to stress which represents a novel therapeutic target for modulation of the hypothalamic-pituitary-adrenal (HPA) axis. Thus, the HPA axis may have important clinical implications for seizure control and imply use of anticonvulsants that influence this neuronal pathway. Copyright 2012 Elsevier Inc. All rights reserved.
HOITZMAN CW,TROTMAN HD,GOULDING SM,et al.Stress and neurodevelopmental processes in the emergence of psychosis[J].Neuroscience,2013,249(26):172-191.
The notion that stress plays a role in the etiology of psychotic disorders, especially schizophrenia, is longstanding. However, it is only in recent years that the potential neural mechanisms mediating this effect have come into sharper focus. The introduction of more sophisticated models of the interplay between psychosocial factors and brain function has expanded our opportunities for conceptualizing more detailed psychobiological models of stress in psychosis. Further, scientific advances in our understanding of adolescent brain development have shed light on a pivotal question that has challenged researchers; namely, why the first episode of psychosis typically occurs in late adolescence/young adulthood. In this paper, we begin by reviewing the evidence supporting associations between psychosocial stress and psychosis in diagnosed patients as well as individuals at clinical high risk for psychosis. We then discuss biological stress systems and examine changes that precede and follow psychosis onset. Next, research findings on structural and functional brain characteristics associated with psychosis are presented; these findings suggest that normal adolescent neuromaturational processes may go awry, thereby setting the stage for the emergence of psychotic syndromes. Finally, a model of neural mechanisms underlying the pathogenesis of psychosis is presented and directions for future research strategies are explored.
LOVEJOYD,CHANG BS,LOVEJOY NR,et al.Molecular evolution of GPCRs:CRH/CRH receptors[J].Mol Endocrinol,2014,52(3):43-60.
Corticotrophin-releasing hormone (CRH) is the pivotal neuroendocrine peptide hormone associated with the regulation of the stress response in vertebrates. However, CRH-like peptides are also found in a number of invertebrate species. The origin of this peptide can be traced to a common ancestor of lineages leading to chordates and to arthropods, postulated to occur some 500 million years ago. Evidence indicates the presence of a single CRH-like receptor and a soluble binding protein system that acted to transduce and regulate the actions of the early CRH peptide. In vertebrates, genome duplications led to the divergence of CRH receptors into CRH1 and CRH2 forms in tandem with the development of four paralogous ligand lineages that included CRH; urotensin I/urocortin (Ucn), Ucn2 and Ucn3. In addition, taxon-specific genome duplications led to further local divergences in CRH ligands and receptors. Functionally, the CRH ligand-receptor system evolved initially as a molecular system to integrate early diuresis and nutrient acquisition. As multicellular organisms evolved into more complex forms, this ligand-receptor system became integrated with the organismal stress response to coordinate homoeostatic challenges with internal energy usage. In vertebrates, CRH and the CRH1 receptor became associated with the hypothalamo-pituitary-adrenal/interrenal axis and the initial stress response, whereas the CRH2 receptor was selected to play a greater role in diuresis, nutrient acquisition and the latter aspects of the stress response.
KOVACS KJ.CRH:the link between hormonal-metabolic and behavioral responses to stress[J].Chem Neur,2013,54(7):25-33.
Two major and mutually interconnected brain systems are recruited during stress reaction. One is the hypothalamic paraventricular nucleus (PVH) and the second is the extended amygdala. PVH governs the neuroendocrine stress response while CeA regulates most of the autonomic and behavioral stress reactions. The common neurohormonal mediator of these responses is the corticotropin-releasing hormone, CRH, which is expressed in both centers. CRH belongs to a larger family of neuropeptides that also includes urocortins 1, 2, and 3 all have different affinity toward the two types of CRHR receptors and have been implicated in regulation of stress and HPA axis activity. One functionally relevant aspect of CRH systems is their differential regulation by glucocorticoids. While corticosterone inhibits CRH transcription in the PVH, stress-induced glucocorticoids stimulate CRH expression in the extended amygdala. This review summarizes past and recent findings related to CRH gene regulation and its involvement in the neuroendocrine, autonomic and behavioral stress reaction.
ALEVIZOSM,KARAGKOUNIA,PANGIOTIDOUS,et al.Stress triggers coronary mast cells leading to cardiac events[J].Ann Allergy Asthma Immunol,2014,112(4):309-316.
Abstract OBJECTIVE: Stress precipitates and worsens not only asthma and atopic dermatitis but also acute coronary syndromes (ACSs), which are associated with coronary inflammation. Evidence linking stress to ACS was reviewed and indicated that activation of coronary mast cells (MCs) by stress, through corticotropin-releasing hormone (CRH) and other neuropeptides, contributes to coronary inflammation and coronary artery disease. DATA SOURCES: PubMed was searched (2005-2013) for articles using the following keywords: allergies, anaphylaxis, anxiety, coronary arteries, coronary artery disease, C-reactive protein, cytokines, chymase, histamine, hypersensitivity, interleukin-6 (IL-6), inflammation, mast cells, myocardial ischemia, niacin, platelet-activating factor, rupture, spasm, statins, stress, treatment, tryptase, and uroctortin. STUDY SELECTIONS: Articles were selected based on their relevance to how stress affects ACS and how it activates coronary MCs, leading to coronary hypersensitivity, inflammation, and coronary artery disease. RESULTS: Stress can precipitate allergies and ACS. Stress stimulates MCs through the activation of high-affinity surface receptors for CRH, leading to a CRH-dependent increase in serum IL-6. Moreover, neurotensin secreted with CRH from peripheral nerves augments the effect of CRH and stimulates cardiac MCs to release IL-6, which is elevated in ACS and is an independent risk factor for myocardial ischemia. MCs also secrete CRH and uroctortin, which induces IL-6 release from cardiomyocytes. The presence of atherosclerosis increases the risk of cardiac MC activation owing to the stimulatory effect of lipoproteins and adipocytokines. Conditions such as Kounis syndrome, mastocytosis, and myalgic encephalopathy/chronic fatigue syndrome are particularly prone to coronary hypersensitivity reactions. CONCLUSION: Inhibition of cardiac MCs may be a novel treatment approach. Copyright 2014 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
, 王晓敏, 周志愉, 温晓梨, 刘志勇
