Corticotropin-Releasing Hormone, Arginine Vasopressin, Gastrin-Releasing Peptide, and Neuromedin B Alterations in Stress-Relevant Brain Regions of Suicides and Control Subjects

2006 ◽  
Vol 59 (7) ◽  
pp. 594-602 ◽  
Author(s):  
Zul Merali ◽  
Pamela Kent ◽  
Lisheng Du ◽  
Pavel Hrdina ◽  
Miklos Palkovits ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Brain Regions ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Gastrin Releasing Peptide ◽  
Control Subjects ◽  
Neuromedin B ◽  
And Control

Consistent Reduction of ACTH responses to stimulation with CRH, Vasopressin and Hypoglycaemia in Patients with Major Depression

1989 ◽  
Vol 155 (4) ◽  
pp. 468-478 ◽  
Author(s):  
Roger G. Kathol ◽  
Richard S. Jaeckle ◽  
Juan F. Lopez ◽  
William H. Meller
Keyword(s):  
Major Depression ◽  
Hpa Axis ◽  
Negative Correlation ◽  
Arginine Vasopressin ◽  
Corticotropin Releasing Hormone ◽  
Hypothalamic Pituitary Adrenal ◽  
Releasing Hormone ◽  
Control Subjects ◽  
Basal Cortisol ◽  
Cortisol Responses

Eleven patients with major depression and 12 control subjects were administered corticotropin-releasing hormone (CRH), aqueous arginine vasopressin (AVP), and insulin hypoglycaemia (IH) to test for differences in hypothalamic–pituitary–adrenal (HPA) axis function. Patients with major depression demonstrated lower ACTH responses to CRH when compared with controls, and a trend toward such after administration of AVP. Despite lower ACTH responses in patients with depression, there were no differences in Cortisol responses to these stimuli. In the CRH and AVP tests, there was no correlation between the basal Cortisol and ACTH responses in either controls or patients, but in the IH test there was a negative correlation between these responses for both groups. The ACTH responses to CRH and AVP were positively correlated in controls and patients. Cortisol responses to all three provocative stimuli were positively correlated in both subject groups. These findings are consistent with the hypothesis that hypothalamic or supra-hypothalamic overactivity may be involved in the development of HPA-axis abnormalities in patients with depression.

scholarly journals Dysregulation of bladder corticotropin-releasing hormone receptor in the pathogenesis of human interstitial cystitis/bladder pain syndrome

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jia-Fong Jhang ◽  
Lori A. Birder ◽  
Yuan-Hong Jiang ◽  
Yung-Hsiang Hsu ◽  
Han-Chen Ho ◽  
...  
Keyword(s):  
Interstitial Cystitis ◽  
Hormone Receptor ◽  
Bladder Wall ◽  
Pain Syndrome ◽  
Bladder Pain Syndrome ◽  
Corticotropin Releasing Hormone ◽  
Bladder Pain ◽  
Releasing Hormone ◽  
Control Subjects ◽  
And Control

AbstractStress is associated with exacerbated symptoms in patients with interstitial cystitis/bladder pain syndrome (IC/BPS). To investigate the mechanism of stress implicated on IC/BPS, we investigated expression of stress-response receptor corticotropin-releasing hormone receptor (CRHR) in bladder from IC/BPS patients. Twenty-three IC/BPS patients with Hunner’s lesion (HIC), 51 IC/BPS patients without Hunner’s lesion (NHIC), and 24 patients with stress urinary incontinence as controls were enrolled. Cystoscopic biopsies of bladder wall including mucosa and submucosa were obtained from all patients. Western blotting was used to investigate the bladder expression of the CRHR1 and CRHR2. Immunochemical staining revealed CRHR1 expression was mainly located in the submucosa while CRHR2 expression was mainly in uroepithelial cells. Compared to control subjects, the CRHR1 expression was significantly higher, while CRHR2 expression was significantly lower in IC/BPS patients. Further analysis of patients with HIC, NHIC, and control subjects showed that bladder in patients with HIC had significantly higher expressions of CRHR1 and significantly lower CRHR2. CRHR2 expression was significantly negatively correlated with O’Leary-Sant score and bladder pain. Our results indicate dysregulation of bladder CRHR1 and CRHR2 in patients with IC/BPS, and suggest CRH signaling may be associated with IC/BPS symptoms.

Release of hypothalamic corticotropin-releasing hormone and arginine-vasopressin by interleukin 1β and αMSH: studies in rats with different susceptibility to inflammatory disease

1993 ◽  
Vol 631 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Piotr Zelazowski ◽  
Vladimir K. Patchev ◽  
Elzbieta B. Zelazowska ◽  
George P. Chrousos ◽  
Philip W. Gold ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Inflammatory Disease ◽  
Interleukin 1Β ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

scholarly journals The Role of Corticotropin-Releasing Hormone at Peripheral Nociceptors: Implications for Pain Modulation

Biomedicines ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 623
Author(s):  
Haiyan Zheng ◽  
Ji Yeon Lim ◽  
Jae Young Seong ◽  
Sun Wook Hwang
Keyword(s):  
Signal Transmission ◽  
Brain Regions ◽  
Pain Modulation ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Inhibitory Function ◽  
Peripheral Pain ◽  
Functional Profiles ◽  
Pituitary Adrenal Axis

Peripheral nociceptors and their synaptic partners utilize neuropeptides for signal transmission. Such communication tunes the excitatory and inhibitory function of nociceptor-based circuits, eventually contributing to pain modulation. Corticotropin-releasing hormone (CRH) is the initiator hormone for the conventional hypothalamic-pituitary-adrenal axis, preparing our body for stress insults. Although knowledge of the expression and functional profiles of CRH and its receptors and the outcomes of their interactions has been actively accumulating for many brain regions, those for nociceptors are still under gradual investigation. Currently, based on the evidence of their expressions in nociceptors and their neighboring components, several hypotheses for possible pain modulations are emerging. Here we overview the historical attention to CRH and its receptors on the peripheral nociception and the recent increases in information regarding their roles in tuning pain signals. We also briefly contemplate the possibility that the stress-response paradigm can be locally intrapolated into intercellular communication that is driven by nociceptor neurons. Such endeavors may contribute to a more precise view of local peptidergic mechanisms of peripheral pain modulation.

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