Sexual dimorphism in stress-induced changes in adrenergic and muscarinic receptor densities in the lung of wild type and corticotropin-releasing hormone-knockout mice

Stress ◽  
2010 ◽  
Vol 13 (1) ◽  
pp. 22-35 ◽  
Author(s):  
Martina Novakova ◽  
Richard Kvetnansky ◽  
Jaromir Myslivecek
Keyword(s):  
Sexual Dimorphism ◽  
Muscarinic Receptor ◽  
Knockout Mice ◽  
Corticotropin Releasing Hormone ◽  
Wild Type ◽  
Releasing Hormone ◽  
Induced Changes

scholarly journals Glucocorticoid-deficient corticotropin-releasing hormone knockout mice maintain glucose requirements but not autonomic responses during repeated hypoglycemia

2006 ◽  
Vol 291 (1) ◽  
pp. E15-E22 ◽  
Author(s):  
Lauren Jacobson ◽  
Tasneem Ansari ◽  
Jessica Potts ◽  
Owen P. McGuinness
Keyword(s):  
Blood Glucose ◽  
Autonomic Failure ◽  
Plasma Catecholamines ◽  
Corticotropin Releasing Hormone ◽  
Wild Type ◽  
Releasing Hormone ◽  
Autonomic Responses ◽  
Hormone Responses ◽  
Acute Hypoglycemia ◽  
Similar Day

Glucocorticoids have been implicated in hypoglycemia-induced autonomic failure but also contribute to normal counterregulation. To determine the influence of normal and hypoglycemia-induced levels of glucocorticoids on counterregulatory responses to acute and repeated hypoglycemia, we compared plasma catecholamines, corticosterone, glucagon, and glucose requirements in male wild-type (WT) and glucocorticoid-deficient, corticotropin-releasing hormone knockout (CRH KO) mice. Conscious, chronically cannulated, unrestrained WT and CRH KO mice underwent a euglycemic (Prior Eu) or hypoglycemic clamp (Prior Hypo) on day 1 followed by a hypoglycemic clamp on day 2 (blood glucose both days, 65 ± 1 mg/dl). Baseline epinephrine and glucagon were similar, and norepinephrine was elevated, in CRH KO vs. WT mice. CRH KO corticosterone was almost undetectable (<1.5 μg/dl) and unresponsive to hypoglycemia. CRH KO glucose requirements were significantly higher during day 1 hypoglycemia despite epinephrine and glucagon responses that were comparable to or greater than those in WT. Hyperinsulinemic euglycemia did not increase hormones or glucose requirements above baseline. On day 2, Prior Hypo WT had significantly higher glucose requirements and significantly lower corticosterone and glucagon responses. Prior Hypo and Prior Eu CRH KO mice had similar day 2 glucose requirements. However, Prior Hypo CRH KO mice had significantly lower day 2 epinephrine and norepinephrine vs. Prior Eu CRH KO and tended to have lower glucagon than on day 1. We conclude that glucocorticoid insufficiency in CRH KO mice correlates with 1) impaired counterregulation during acute hypoglycemia and 2) complex effects after repeated hypoglycemia, neither preventing decreased hormone responses nor worsening glucose requirements.

scholarly journals MeCP2 haplodeficiency and early-life stress interaction on anxiety-like behavior in adolescent female mice

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
María Abellán-Álvaro ◽  
Oliver Stork ◽  
Carmen Agustín-Pavón ◽  
Mónica Santos
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Early Life Stress ◽  
Hypothalamic Nucleus ◽  
Corticotropin Releasing Hormone ◽  
Wild Type ◽  
Releasing Hormone ◽  
Complex Disorders ◽  
Female Mice

Abstract Background Early-life stress can leave persistent epigenetic marks that may modulate vulnerability to psychiatric conditions later in life, including anxiety, depression and stress-related disorders. These are complex disorders with both environmental and genetic influences contributing to their etiology. Methyl-CpG Binding Protein 2 (MeCP2) has been attributed a key role in the control of neuronal activity-dependent gene expression and is a master regulator of experience-dependent epigenetic programming. Moreover, mutations in the MECP2 gene are the primary cause of Rett syndrome and, to a lesser extent, of a range of other major neurodevelopmental disorders. Here, we aim to study the interaction of MeCP2 with early-life stress in variables known to be affected by this environmental manipulation, namely anxiety-like behavior and activity of the underlying neural circuits. Methods Using Mecp2 heterozygous and wild-type female mice we investigated the effects of the interaction of Mecp2 haplodeficiency with maternal separation later in life, by assessing anxiety-related behaviors and measuring concomitant c-FOS expression in stress- and anxiety-related brain regions of adolescent females. Moreover, arginine vasopressin and corticotropin-releasing hormone neurons of the paraventricular hypothalamic nucleus were analyzed for neuronal activation. Results In wild-type mice, maternal separation caused a reduction in anxiety-like behavior and in the activation of the hypothalamic paraventricular nucleus, specifically in corticotropin-releasing hormone-positive cells, after the elevated plus maze. This effect of maternal separation was not observed in Mecp2 heterozygous females that per se show decreased anxiety-like behavior and concomitant decreased paraventricular nuclei activation. Conclusions Our data supports that MeCP2 is an essential component of HPA axis reprogramming and underlies the differential response to anxiogenic situations later in life.

scholarly journals Sexual dimorphism of stress response and immune/ inflammatory reaction: the corticotropin releasing hormone perspective

1995 ◽  
Vol 4 (3) ◽  
pp. 163-174 ◽  
Author(s):  
Nicholas V. Vamvakopoulos
Keyword(s):  
Gene Expression ◽  
Sexual Dimorphism ◽  
Stress Response ◽  
Inflammatory Reaction ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
New Concepts ◽  
Glucocorticoid Administration ◽  
Regulatory Potential ◽  
Key Aspects

This review higlghts key aspects of corticotropin releasing hormone (CRH) biology of potential relevance to the sexual dimorphism of the stress response and immune/inflammatory reaction, and introduces two important new concepts based on the regulatory potential of the human (h) CRH gene: (1) a proposed mechanism to account for the tissue-specific antithetical responses of hCRH gene expression to glucocorticolds, that may also explain the frequently observed antithetical effects of chronic glucocorticoid administration in clinical practice and (2) a heuristic diagram to illustrate the proposed modulation of the stress response and immune/ inflammatory reaction by steroid hormones, from the perspective of the CRH system.

M3-receptor knockout mice: muscarinic receptor function in atria, stomach fundus, urinary bladder, and trachea

2002 ◽  
Vol 282 (5) ◽  
pp. R1443-R1449 ◽  
Author(s):  
Peter W. Stengel ◽  
Masahisa Yamada ◽  
Jürgen Wess ◽  
Marlene L. Cohen
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Muscarinic Receptor ◽  
Knockout Mice ◽  
Smooth Muscle Contraction ◽  
Receptor Activation ◽  
Muscarinic Agonist ◽  
Wild Type ◽  
Atrial Rate ◽  
Stomach Fundus

Negative chronotropic and smooth muscle contractile responses to the nonselective muscarinic agonist carbamylcholine were compared in isolated tissues from M3-muscarinic receptor knockout and wild-type mice. Carbamylcholine (10−8–3.0 × 10−5 M) induced a concentration-dependent decrease in atrial rate that was similar in atria from M3-receptor knockout and wild-type mice, indicating that M3 receptors were not involved in muscarinic receptor-mediated atrial rate decreases. In contrast, the M3 receptor was a major muscarinic receptor involved in smooth muscle contraction of stomach fundus, urinary bladder, and trachea, although differences existed in the extent of M3-receptor involvement among the tissues. Contraction to carbamylcholine was virtually abolished in urinary bladder from M3-receptor knockout mice, suggesting that contraction was predominantly due to M3-receptor activation. However, ∼50–60% maximal contraction to carbamylcholine occurred in stomach fundus and trachea from M3-receptor knockout mice, indicating that contraction in these tissues was also due to M2-receptor activation. High concentrations of carbamylcholine relaxed the stomach fundus from M3-receptor knockout mice by M1-receptor activation. Thus M3-receptor knockout mice provided unambiguous evidence that M3 receptors 1) play no role in carbamylcholine-induced atrial rate reduction, 2) are the predominant receptor mediating carbamylcholine-induced urinary bladder contractility, and 3) share contractile responsibility with M2 receptors in mouse stomach fundus and trachea.

Corticotropin-releasing hormone mimics stress-induced colonic epithelial pathophysiology in the rat

1999 ◽  
Vol 277 (2) ◽  
pp. G391-G399 ◽  
Author(s):  
Javier Santos ◽  
Paul R. Saunders ◽  
Nico P. M. Hanssen ◽  
Ping-Chang Yang ◽  
Derrick Yates ◽  
...  
Keyword(s):  
Mast Cells ◽  
Stress Responses ◽  
Restraint Stress ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Ussing Chambers ◽  
Ion Secretion ◽  
Epithelial Physiology ◽  
Induced Changes

We examined the effect of stress on colonic epithelial physiology, the role of corticotropin-releasing hormone (CRH), and the pathways involved. Rats were restrained or injected intraperitoneally with CRH or saline. Colonic segments were mounted in Ussing chambers, in which ion secretion and permeability (conductance and probe fluxes) were measured. To test the pathways involved in CRH-induced changes, rats were pretreated with hexamethonium, atropine, bretylium, doxantrazole, α-helical CRH-(9—41) (all intraperitoneally), or aminoglutethimide (subcutaneously). Restraint stress increased colonic ion secretion and permeability to ions, the bacterial peptide FMLP, and horseradish peroxidase (HRP). These changes were prevented by α-helical CRH-(9—41) and mimicked by CRH (50 μg/kg). CRH-induced changes in ion secretion were abolished by α-helical CRH-(9—41), hexamethonium, atropine, or doxantrazole. CRH-stimulated conductance was significantly inhibited by α-helical CRH-(9—41), hexamethonium, bretylium, or doxantrazole. CRH-induced enhancement of HRP flux was significantly reduced by all drugs but aminoglutethimide. Peripheral CRH reproduced stress-induced colonic epithelial pathophysiology via cholinergic and adrenergic nerves and mast cells. Modulation of stress responses may be relevant to the management of colonic disorders.

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