scholarly journals Corticotropin-releasing hormone receptor antagonists

2006 ◽  
Vol 155 (suppl_1) ◽  
pp. S85-S91 ◽  
Author(s):  
E Zoumakis ◽  
D K Grammatopoulos ◽  
G P Chrousos
Keyword(s):  
Immune Responses ◽  
Stress Responses ◽  
Preterm Labor ◽  
Anxiety And Depression ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Physiological Processes ◽  
Crh Receptors ◽  
Potential Use

Corticotropin-releasing hormone (CRH), CRH-related peptides, and CRH receptors play major roles in coordinating the behavioral, endocrine, autonomic, and immune responses to stress. The wide influence of the CRH system on physiological processes in both brain and periphery implicates the respective peptides in the pathophysiology of numerous disorders characterized by dysregulated stress responses. The potential use of CRH antagonists is presently under intense investigation. Selective antagonists have been used experimentally to elucidate the role of CRH-related peptides in disease processes, such as anxiety and depression, sleep disorders, addictive behavior, inflammatory disorders, acute and chronic neurodegeneration, and preterm labor.

scholarly journals Corticotropin-releasing hormone signals adversity in both the placenta and the brain: regulation by glucocorticoids and allostatic overload

1999 ◽  
Vol 161 (3) ◽  
pp. 349-356 ◽  
Author(s):  
J Schulkin
Keyword(s):  
Gene Expression ◽  
Preterm Labor ◽  
Functional Role ◽  
Stria Terminalis ◽  
Corticotropin Releasing Hormone ◽  
Bed Nucleus ◽  
Releasing Hormone ◽  
The Brain ◽  
Hormone Signals

Glucocorticoids regulate corticotropin-releasing hormone (CRH) gene expression in the placenta and the brain. In both the placenta and two extrahypothalamic sites in the brain (the amygdala and the bed nucleus of the stria terminalis), glucocorticoids elevate CRH gene expression. One functional role of the elevation of CRH by glucocorticoids may be to signal adversity. When CRH is over-expressed in the placenta, it may indicate that the pregnancy is in danger, and preterm labor may result. When CRH is over-expressed in the brains of animals, they may become more fearful. Both situations possibly reflect allostatic mechanisms and vulnerability to allostatic overload, a condition in which biological tissue may be compromised.

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.

Dissecting the role of Corticotropin-releasing hormone receptor type 1 in Alzheimer's Disease

2011 ◽  
Vol 44 (06) ◽  
Author(s):  
K Lerche ◽  
M Willem ◽  
K Kleinknecht ◽  
C Romberg ◽  
U Konietzko ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hormone Receptor ◽  
Receptor Type ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

The role of corticotropin-releasing hormone (CRH) family in tumor

Neoplasma ◽  
2021 ◽  
Author(s):  
Su-Qin Yi ◽  
Jia-Xing An ◽  
Cheng-Cheng Liao ◽  
Sha Lei ◽  
Hai Jin ◽  
...  
Keyword(s):  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

An Overview on the Role of miR-451 in Lung Cancer: Diagnosis, Therapy, and Prognosis

MicroRNA ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Saiedeh Razi Soofiyani ◽  
Kamram Hosseini ◽  
Alireza Soleimanian ◽  
Liela Abkhooei ◽  
Akbar Mohammad Hoseini ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Diagnosis ◽  
Lung Tumor ◽  
Expression Patterns ◽  
Lung Cancer Diagnosis ◽  
Physiological Processes ◽  
Cell Proliferation Inhibition ◽  
Diagnosis Therapy ◽  
Potential Use

: MicroRNAs (miRNAs) are highly conserved non-coding RNAs involved in many physiological processes such as cell proliferation, inhibition, development of apoptosis, differentiation, suppresses tumorigenicity, and regulating cell growth. The description of the alterations of miRNA expression patterns in cancers will be helpful to recognize biomarkers for early detection and possible therapeutic intervention in the treatment of cancers. Recent studies have shown that miR-451 is broadly dysregulated in lung cancer and is a crucial agent in lung tumor progression. This review summarizes recent advances of the potential role of miR-451 in lung cancer diagnosis, prognosis, and treatment and provides an insight into the potential use of miR-451 for the development of advanced therapeutic methods in lung cancer.

Stress and Anxiety in Schizophrenia and Depression: Glucocorticoids, Corticotropin-Releasing Hormone and Synapse Regression

2008 ◽  
Vol 42 (12) ◽  
pp. 995-1002 ◽  
Author(s):  
Maxwell R. Bennett Ao
Keyword(s):  
Neural Networks ◽  
Nmda Receptors ◽  
Receptor Activation ◽  
Stressful Events ◽  
Childhood And Adolescence ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Spine Stability ◽  
The Stability ◽  
Crh Receptors

Stress during childhood and adolescence has implications for the extent of depression and psychotic disorders in maturity. Stressful events lead to the regression of synapses with the loss of synaptic spines and in some cases whole dendrites of pyramidal neurons in the prefrontal cortex, a process that leads to the malfunctioning of neural networks in the neocortex. Such stress often shows concomitant increases in the activity of the hypothalamic–pituitary–adrenal system, with a consequent elevated release of glucocorticoids such as cortisol as well as of corticotropin-releasing hormone (CRH) from neurons. It is very likely that it is these hormones, acting on neuronal and astrocyte glucocorticoid receptors (GRs) and CRH receptors, respectively, that are responsible for the regression of synapses. The mechanism of such regression involves the loss of synaptic spines, the stability of which is under the direct control of the activity of N-methyl-d-aspartate (NMDA) receptors on the spines. Glutamate activates NMDA receptors, which then, through parallel pathways, control the extent in the spine of the cytoskeletal protein F-actin and so spine stability and growth. Both GR and CRH receptors in the spines can modulate NMDA receptors, reducing their activation by glutamate and hence spine stability. In contrast, glucocorticoids, probably acting on nerve terminal and astrocyte GRs, can release glutamate, so promoting NMDA receptor activation. It is suggested that spine stability is under dual control by glucocorticoids and CRH, released during stress to change the stability of synaptic spines, leading to the malfunctioning of cortical neural networks that are involved in depression and psychoses.

scholarly journals The role of corticotropin-releasing hormone in neuroendocrine-immune interactions

1997 ◽  
Vol 2 (5) ◽  
pp. 368-372 ◽  
Author(s):  
E L Webster ◽  
I J Elenkov ◽  
G P Chrousos
Keyword(s):  
Corticotropin Releasing Hormone ◽  
Releasing Hormone
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