Comparison of central administration of corticotropin-releasing hormone and urocortin on food intake, conditioned taste aversion, and c-Fos expression☆

Central administration of corticotropin-releasing hormone (CRH) is known to inhibit food intake and stimulate pituitary oxytocin (OT) secretion in rats. These experiments addressed the possibility that the inhibition of food intake that follows central CRH administration is mediated through oxytocinergic pathways. Male food-deprived rats, with stable baseline food intakes after intracerebroventricular (icv) injections of artificial cerebrospinal fluid, received 150 pmol of CRH icv. Food intake was inhibited by 62 +/- 5% during a 90-min test period. Pretreatment with 9 nmol of the OT antagonist [d(CH2)5, Tyr(Me)2, Orn8]vasotocin icv completely eliminated the inhibition of food intake produced by icv CRH. In contrast, pretreatment with the OT-receptor antagonist did not significantly alter pituitary secretion of adrenocorticotropic hormone and OT stimulated by icv CRH. The results of these experiments implicate OT as a possible central mediator of CRH-induced anorexias in rats, particularly those that are accompanied by stimulation of neurohypophysial OT secretion.

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Central administration of growth hormone-releasing hormone and corticotropin-releasing hormone stimulate downstream movement and thyroxine secretion in fall-smolting coho salmon (Oncorhynchus kisutch)

General and Comparative Endocrinology ◽

10.1016/j.ygcen.2010.04.007 ◽

2010 ◽

Vol 168 (1) ◽

pp. 82-87 ◽

Cited By ~ 13

Author(s):

Daisuke Ojima ◽

Munehico Iwata

Keyword(s):

Growth Hormone ◽

Coho Salmon ◽

Oncorhynchus Kisutch ◽

Growth Hormone Releasing Hormone ◽

Central Administration ◽

Corticotropin Releasing Hormone ◽

Releasing Hormone ◽

Downstream Movement

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Gfral-expressing Neurons Suppress Food Intake via Aversive Pathways

10.1101/2020.05.11.088773 ◽

2020 ◽

Author(s):

Paul V. Sabatini ◽

Henriette Frikke-Schmidt ◽

Joe Arthurs ◽

Desiree Gordian ◽

Anita Patel ◽

...

Keyword(s):

Gastric Emptying ◽

Food Intake ◽

Taste Aversion ◽

Conditioned Taste Aversion ◽

Mechanisms Of Action ◽

Parabrachial Nucleus ◽

Gastric Physiology ◽

Anorexigenic Peptide ◽

Artificial Activation ◽

Meal Ingestion

AbstractTo determine the function and mechanisms of action for hindbrain neurons that express GFRAL, the receptor for the anorexigenic peptide, GDF-15, we generated Gfralcre and conditional GfralCreERT mice. While signals of infection or pathophysiologic states (rather than meal ingestion) stimulate GFRAL neurons, the artificial activation of GfralCre- expressing neurons inhibited feeding, decreased gastric emptying, and promoted a conditioned taste aversion (CTA). Additionally, activation of the smaller population of GFRAL neurons captured by the GfralCreERT allele decreased gastric emptying and produced a CTA without suppressing food intake, suggesting that GFRAL neurons primarily modulate gastric physiology and stimulate aversive responses. GFRAL neurons most strongly innervated the parabrachial nucleus (PBN), where they targeted CGRP-expressing (CGRPPBN) neurons. Silencing CGRPPBN neurons abrogated the aversive and anorexic effects of GDF-15. These findings suggest that GFRAL neurons link non-meal-associated, pathophysiologic signals to the aversive suppression of nutrient uptake and absorption.

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Corticotropin-releasing hormone-binding protein in brain and pituitary of food-deprived obese (fa/fa) Zucker rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.277.6.r1749 ◽

1999 ◽

Vol 277 (6) ◽

pp. R1749-R1759 ◽

Cited By ~ 3

Author(s):

Elena Timofeeva ◽

Yves Deshaies ◽

Frédéric Picard ◽

Denis Richard

Keyword(s):

Food Intake ◽

Food Deprivation ◽

Binding Protein ◽

Mrna Level ◽

Zucker Rats ◽

Pituitary Cells ◽

Dorsal Part ◽

Corticotropin Releasing Hormone ◽

Releasing Hormone ◽

Ad Libitum

The present study was conducted to verify whether experimental conditions such as obesity and food deprivation, which promote food intake and reduce thermogenesis, could modify the expression of the corticotropin-releasing hormone (CRH)-binding protein (BP) in the rat brain. In situ hybridization, histochemistry, and immunohistochemistry were used to assess the expression of CRH-BP in lean ( Fa/?) and obese ( fa/fa) Zucker rats that were fed ad libitum, food deprived for 24 h, or food deprived for 24 h and refed for 6 h. In both lean and obese rats, food deprivation led to a reduction in body weight that was accompanied by a reversible increase in plasma corticosterone levels. Food deprivation and, to a lesser degree, obesity induced the expression of CRH-BP mRNA in the dorsal part of the medial preoptic area (MPOA). This induction of the CRH-BP gene led to by food deprivation was confirmed by the appearance in the dorsal part of the MPOA of neurons immunoreactive to CRH-BP. Food deprivation (in particular) and obesity also increased the levels of CRH-BP mRNA in the basolateral amygdala (BLA). The enhanced CRH-BP expression in the MPOA and BLA in response to food deprivation was reversed by refeeding. In lean Fa/? rats, the CRH-BP mRNA level in the pituitary cells was significantly decreased after food deprivation and restored after refeeding. When food was provided ad libitum, the number of cells expressing CRH-BP in the anterior pituitary was significantly higher in lean rats than in obese animals. Food deprivation for 24 h decreased dramatically the number of pituitary cells expressing CRH-BP in lean rats. Altogether, the present results demonstrate that food deprivation and, to a lesser extent, obesity can selectively affect the expression of CRH-BP. Given both the inactivating effect of CRH-BP on the CRH system and the potential roles played by the MPOA and BLA in the thermogenic and anorectic effects of CRH, it can be argued that the induction of the CRH-BP gene in obesity and after food deprivation occurs as a mechanism to reduce energy expenditure and to stimulate food intake.

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