scholarly journals Species and sex differences in brain distribution of corticotropin-releasing factor receptor subtypes 1 and 2 in monogamous and promiscuous vole species

2005 ◽  
Vol 487 (1) ◽  
pp. 75-92 ◽  
Author(s):  
Miranda M. Lim ◽  
Hemanth P. Nair ◽  
Larry J. Young
Keyword(s):  
Sex Differences ◽  
Corticotropin Releasing Factor ◽  
Receptor Subtypes ◽  
Brain Distribution ◽  
Vole Species

scholarly journals Corticotropin-Releasing Factor Receptor Binding in the Amygdala Changes Across Puberty in a Sex-Specific Manner

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 5701-5705 ◽  
Author(s):  
Jill M. Weathington ◽  
Bradley M. Cooke
Keyword(s):  
Sex Differences ◽  
Receptor Binding ◽  
Specific Binding ◽  
Stress Sensitivity ◽  
Corticotropin Releasing Factor ◽  
Receptor Subtypes ◽  
Medial Amygdala ◽  
Adult Males ◽  
Adult Rats ◽  
Hypothalamic Pituitary Adrenal

Abstract Corticotropin-releasing factor receptors type 1 (CRF1) and type 2 (CRF2) have complementary roles in controlling the hypothalamic-pituitary-adrenal (HPA) axis. Because CRF receptors are expressed in sex steroid-sensitive areas of the forebrain, they may contribute to sex-specific patterns of stress sensitivity and susceptibility to stress-related mood disorders, which are more frequent in women. To determine whether CRF receptors vary as a function of age and/or sex, we measured receptor binding in the amygdala of male and female, prepubertal and adult rats. Both receptor subtypes demonstrated age- and sex-specific binding patterns. In the basolateral amygdala and posteroventral medial amygdala, CRF1 binding decreased in males and increased in females after puberty, there, CRF2 binding increased in males and was unchanged in females. In the posterodorsal medial amygdala, CRF1 binding was unchanged across puberty, whereas CRF2 binding increased across puberty far more in males than in females. Binding was lowest overall in the central amygdala; there, CRF1 was unchanged while CRF2 binding increased across puberty only in males. Thus, in all four examined areas across prepuberty to adulthood, CRF2 binding increased far more in males than in females and resulted in significantly more binding in adult males than in adult females. These sex-specific developmental patterns are consistent with sex differences in hypothalamic-pituitary-adrenal responsiveness and may thus contribute to sex differences in mood disorder susceptibility.

scholarly journals Sex differences in the corticotropin‐releasing factor receptor and its regulation by stress

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Debra A Bangasser ◽  
Thelma T. Bethea ◽  
Ioannis Parastatidis ◽  
Rita J Valentino
Keyword(s):  
Sex Differences ◽  
Corticotropin Releasing Factor

scholarly journals Sex Differences in the Subcellular Distribution of Corticotropin-Releasing Factor Receptor 1 in the Rat Hippocampus following Chronic Immobilization Stress

Neuroscience ◽  
2018 ◽  
Vol 383 ◽  
pp. 98-113 ◽  
Author(s):  
Helena R. McAlinn ◽  
Batsheva Reich ◽  
Natalina H. Contoreggi ◽  
Renata Poulton Kamakura ◽  
Andreina G. Dyer ◽  
...  
Keyword(s):  
Sex Differences ◽  
Subcellular Distribution ◽  
Immobilization Stress ◽  
Corticotropin Releasing Factor ◽  
Rat Hippocampus ◽  
Chronic Immobilization Stress

scholarly journals Antagonism of specific corticotropin-releasing factor receptor subtypes selectively modifies weight loss in restrained rats

2008 ◽  
Vol 295 (6) ◽  
pp. R1762-R1773 ◽  
Author(s):  
Christina Chotiwat ◽  
Ruth B. S. Harris
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Third Ventricle ◽  
Corticotropin Releasing Factor ◽  
Receptor Subtypes ◽  
Mild Stress ◽  
Sustained Reduction ◽  
Corticosterone Response ◽  
Poststress Period ◽  
Corticosterone Release

Rats exposed to 3 h of restraint stress on each of 3 days (RRS) lose weight on the days of RRS and gain weight at the same rate as controls after stress ends, but do not return to the weight of controls. RRS rats also show an exaggerated endocrine response to subsequent novel stressors. Studies described here tested the effects of corticotropin-releasing factor receptor (CRFR) antagonism on RRS-induced weight loss, hypophagia, and corticosterone release during mild stress in the postrestraint period. Weight loss was not prevented by either peripheral or third-ventricle administration of a CRFR1 antagonist, antalarmin, before each restraint. Antalarmin did, however, allow recovery of body weight in the poststress period. Third-ventricle administration of a CRFR2 antagonist, antisauvagine 30, had no effect in RRS rats but caused sustained weight loss in control animals. Surprisingly, third-ventricle administration of the nonselective CRFR antagonist, astressin, caused hypophagia and reversible weight loss in control rats. It had no effect in RRS rats. None of the antagonists modified the corticosterone response to RRS or to mild stress in the post-RRS period, but antalarmin suppressed corticosterone during the period of restraint in Control rats. These results suggest that CRFR1 activation is required for the initiation of events that lead to a prolonged down-regulation of body weight in RRS rats. The sustained reduction in body weight is independent of the severity of hypophagia on the days of restraint and of RRS-induced corticosterone release.

scholarly journals Sex differences in corticotropin releasing factor-evoked behavior and activated networks

2016 ◽  
Vol 73 ◽  
pp. 204-216 ◽  
Author(s):  
Kimberly R. Wiersielis ◽  
Brittany Wicks ◽  
Hannah Simko ◽  
Sarah R. Cohen ◽  
Sabina Khantsis ◽  
...  
Keyword(s):  
Sex Differences ◽  
Corticotropin Releasing Factor

scholarly journals Acyloxyacyl Hydrolase Modulates the Gut Microbiome Through Transcriptional Regulators of Corticotropin-Releasing Factor

2021 ◽  
Author(s):  
Afrida Rahman-Enyart ◽  
Lizath M. Aguiniga ◽  
Wenbin Yang ◽  
Ryan E. Yaggie ◽  
Bryan White ◽  
...  
Keyword(s):  
Sex Differences ◽  
Pelvic Pain ◽  
Gut Microbiome ◽  
Transcriptional Regulators ◽  
Corticotropin Releasing Factor ◽  
Conditional Knockout ◽  
Peroxisome Proliferator ◽  
Bladder Pain ◽  
Acyloxyacyl Hydrolase ◽  
Deficient Mice

ABSTRACTGut microbiome-host interactions play a crucial role in health and disease. Altered gut microbiome composition has been observed in patients with interstitial cystitis/bladder pain syndrome (IC/BPS), a disorder characterized by pelvic pain, voiding dysfunction, and often co-morbid with anxiety/depression. We recently showed that mice deficient for acyloxyacyl hydrolase (AOAH) mimic pelvic pain symptoms and comorbidities of IC/BPS and also exhibit gut dysbiosis. In addition, we previously identified that the conditional knockout (cKO) of two transcriptional regulators of the gene encoding corticotropin-releasing factor, Crf, that are downstream of AOAH, aryl hydrocarbon receptor (AhR) and peroxisome proliferator-activated receptor-γ (PPARγ), alleviate anxiety/depressive and voiding phenotypes of AOAH-deficient mice. Here, we examined the effects of AhR and PPARγ in CRF-expressing cells on the dysbiosis of AOAH-deficiency. AOAH-deficient mice with cKO of PPARγ and AhR/PPARγ exhibited reduced pelvic allodynia compared to AOAH-deficient mice, suggesting a role for PPARγ in regulating pelvic pain. 16S rRNA sequencing of fecal stool from female AOAH-deficient mice with a cKO of AhR and/or PPARγ in CRF-expressing cells identified altered gut microbiota distinct from AOAH-deficient stool. The cKO of AhR and PPARγ showed improved cecum barrier function in females compared to AOAH-deficient mice, whereas males were primarily affected by PPARγ, suggesting sex differences in gut responses. Pair-wise comparison of microbiota also suggested sex differences in response to AOAH-deficiency and conditional knockout of AhR and PPARγ. Our findings suggest that the dysbiosis and leaky gut of AOAH deficiency is mediated by AhR and PPARγ in CRF-expressing cells and reveal a novel mechanism and therapeutic targets for pelvic pain.

scholarly journals Functional and anatomical characterization of corticotropin-releasing factor receptor subtypes of the rat spinal cord involved in somatic pain relief

2021 ◽  
Author(s):  
Shaaban Mousa ◽  
Mohammed Shaqura ◽  
Baled Khalefa ◽  
Li Li ◽  
Mohammed Al-madol ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Western Blot ◽  
Opioid Receptor ◽  
Radioligand Binding ◽  
Corticotropin Releasing Factor ◽  
Receptor Subtypes ◽  
Inhibitory Interneurons ◽  
Rat Spinal Cord ◽  
Somatic Pain ◽  
Antinociceptive Effects

Abstract Corticotropin-releasing factor (CRF) orchestrates our body’s response to stressful stimuli. Pain is often stressful and counterbalanced by activation of CRF receptors along the nociceptive pathway, although the involvement of the CRF receptors of subtypes 1 and/or 2 (CRF-R1 and CRF-R2, respectively) in CRF-induced analgesia remains controversial. This study aimed to examine CRF-R1 and CRF-R2 expression within spinal cord of rats with Freund’s complete adjuvant-induced hindpaw inflammation using reverse transcriptase polymerase chain reaction, Western blot, radioligand binding, and immunofluorescence confocal analysis, Western blot, immunohistochemistry, and radioligand binding. Moreover, paw pressure algesiometry examined antinociceptive effects of intrathecal (i.t.) CRF and their possible antagonism through CRF-R1 and/or CRF-R2 selective antagonists as well as opioid receptor antagonist naloxone. Our results demonstrated mainly CRF-R2 mRNA, protein, binding sites and immunoreactivity in dorsal horn of rat spinal cord. In parallel, i.t. CRF as well as CRF-R2 agonists elicited potent antinociceptive effects which are dose-dependent and antagonized exclusively by i.t. CRF-R2 (K41498), but not CRF-R1 (NBI35965) antagonist. Moreover, i.t. CRF elicited inhibition of somatic pain that was dose-dependently reversed by the opioid antagonist naloxone. Consistently, double immunofluorescence confocal microscopy showed CRF-R2 on enkephalin (ENK) containing inhibitory interneurons in close opposition of incoming, mu-opioid receptor-immunoreactive nociceptive neurons but not on pre- nor on postsynaptic sensory neurons of the spinal cord. Taken together, these findings suggest that i.t. CRF or CRF-R2 agonist inhibits inflammatory somatic pain which occurs most predominantly through CRF-R2 receptors located on spinal enkephalinergic inhibitory interneurons resulting in endogenous opioid-mediated pain inhibition.

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