CRF antagonist partially reverses CRF- and stress-induced effects on feeding

Krahn, Dean D.; Gosnell, Blake A.; Grace, Martha K.; Levine, Allen S.

doi:10.1016/0361-9230(86)90233-9

Cited by 288 publications

(137 citation statements)

References 12 publications

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“…6 Although the effects of exogenous CRH or different stress-paradigms on neuronal activity, autonomic system and behavior may be blocked by centrally administred ahelical CRH, 14 -17 the receptor-antagonist alone has been found to be without intrinsic activity on food intake and body weight. 18,19 Although we did observe a small reduction in food intake in the group of animals treated with a-helical CRH, possibly due to an intrinsic activity of the agonist, body weight was unaffected. Compared to control animals (saline i.p.=saline i.c.v.…”

Section: Discussionmentioning

confidence: 73%

“…At the beginning of the experiment, the animals were 12 weeks old and weighed between 300 and 400 g. The animals were kept in single cages at a constant room temperature of 23 C under a 12 h light and dark cycle and were allowed to adapt to the housing conditions prior the surgery for at least 4 days. The dosages of a-helical CRH and fluvoxamine have been shown to be effective by other authors 12 and have been tested by us in a pilot study.…”

Section: Methodsmentioning

confidence: 99%

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The effects of the selective serotonin reuptake-inhibitor fluvoxamine on body weight in Zucker rats are mediated by corticotropin-releasing hormone

et al. 2001

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Brain serotonin plays a crucial role in the regulation of food intake and body weight homeostasis. Previous data suggest an interaction with corticotropin-releasing hormone (CRH). To further examine the interaction between these neurotransmitters, the selective serotonin reuptake-inhibitor (SSRI) fluvoxamine was given intraperitoneally in fa=fa Zucker rats with and without the CRH-receptor-antagonist a-helical CRH administered intracerebroventriculary (i.c.v.). The saline treated animals gained weight. Fluvoxamine led to a significant weight loss while not affecting food intake. Furthermore, insulin levels in this animal model were reduced following fluvoxamine administration. These effects were antagonized by a-helical CRH and are thus most likely mediated via CRH or CRH-like peptides. International Journal of Obesity (2001) IntroductionSelective serotonin reuptake inhibitors (SSRI) are commonly used as drug treatment in depressive disorders. These drugs are well known to centrally affect food intake and body weight homeostasis. This is in accordance with experimental data, demonstrating strong anorectic properties of serotonin when injected into the paraventricular nucleus (PVN) and other hypothalamic areas. 1,2 In the present study we focussed on anorectic properties of the ssri fluvoxamine, which is more specific for serotonin when compared to other compounds of this group of drugs, eg fluoxetine, exerting less effects on the reuptake of noradrenaline. 3 Previous data suggest that, within the PVN, serotonin and corticotropin releasing hormone (CRH) interact to alter food intake and enhanced CRH synthesis has been shown in this particular nucleus following serotonin injection. 4,5 In addition, a stimulating effect of D-fenfluramine, a serotoninreleasing agent, on neuronal activation of CRH expressing cells in the PVN has been demonstrated. 6 CRH clearly possesses anorectic properties, when injected centrally. 7 A causal relationship between the neurotransmitter serotonin and the neuropeptide CRH has, as yet, not been demonstrated. In addition to its anorectic actions, CRH stimulates brown adipose tissue metabolism via activation of the sympathetic nervous system in rodents, when applied centrally, 8,9 potentially causing an increase in energy expenditure.In fa=fa Zucker-rats, CRH 2 -receptor mRNA is reduced in the ventromedial hypothalamus (VMH), suggesting a possible involvement of CRH-neurons in the reduced energy expenditure in this genotype; 10 in addition the hyperinsulinemia in these animals, which is ascribed to an increased activity of vagal efferents to the pancreas, 11 is reduced after local application of CRH to the VMH.This study was aimed at further investigating the nature of brain serotonin and CRH interaction in the control of body weight, which has not been studied before in a long-term in vivo experiment. MethodsChloral hydrate and a-helical CRH were purchased from

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Section: Discussionmentioning

confidence: 73%

Section: Methodsmentioning

confidence: 99%

The effects of the selective serotonin reuptake-inhibitor fluvoxamine on body weight in Zucker rats are mediated by corticotropin-releasing hormone

et al. 2001

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“…High levels of ectopic CRH expression in transkaryotic rats caused marked adrenal cortical hyperplasia and anterior pituitary corticotrope hyperplasia and hypertrophy (Asa et al 1992;Hammer et al 1992). Finally, hypersecretion of CRH is thought to play a role in clinical depression and anorexia nervosa, suggesting that animals with increased CRH levels would exhibit altered motor activity, feeding, and sexual behavior (Gold and Chrousos 1985;Krahn et al 1986Krahn et al , 1990Levine et al 1983;Nakahara 1983;Nemeroff et al 1984;Sirinathsinghji et al 1983;Sutton et al 1982).…”

mentioning

confidence: 99%

Corticotropin-releasing hormone (Crh) maps to mouse Chromosome 3

et al. 1993

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“…Hypothalamic NPY and CRH influence food intake, since they elicit, respectively block, feeding in rats (Krahn et al, 1986). In one study, CRH was observed to block NPYinduced feeding in rats, suggesting that CRH overrides the effect of NPY in this behavioral aspect (Heinrichs et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…The role of CRH in mood disorders has been extensively studied (for a review, see Holsboer, 2000) and was not the primary subject of this investigation. However, since CRH, in opposition to NPY, blocks feeding and has proconvulsant effects in rats (Brunson et al, 1998;Krahn et al, 1986), it was of interest to study it in this particular context. Galanin, in similarity to NPY, induces food ingestion in satiated rats and dampens the development of experimental epilepsy (Halford, 2001;Kokaia et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Topiramate Normalizes Hippocampal NPY-LI in Flinders Sensitive Line ‘Depressed’ Rats and Upregulates NPY, Galanin, and CRH-LI in the Hypothalamus: Implications for Mood-Stabilizing and Weight Loss-Inducing Effects

Husum

Kammen

Termeer

et al. 2003

Neuropsychopharmacol

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Topiramate is currently used in the treatment of epilepsy, but this anticonvulsant drug has also been reported to exert mood-stabilizing effects and induce weight loss in patients. Neuropeptide Y (NPY) is abundantly and widely distributed in the mammalian central nervous system and centrally administered NPY markedly reduces pharmacologically induced seizures and induces antidepressant-like activity as well as feeding behavior. Two other peptides, galanin and corticotropin-releasing hormone (CRH), have also been proposed to play a modulatory role in mood, appetite, and seizure regulation. Consequently, we investigated the effects of single and repeated topiramate (10 days, once daily: 40 mg/kg i.p.) or vehicle treatment in 'depressed' flinders sensitive line (FSL) and control Flinders resistant line (FRL) rats on brain regional peptide concentrations of NPY, galanin, and CRH. The handling associated with repeated injections reduced hippocampal levels of NPY-and galanin-like immunoreactivities (LI) while NPY-and CRH-LI levels were increased in the hypothalamus, regardless of strain or treatment. In the hippocampus, concentrations of NPY-LI, galanin-LI, and CRH-LI were lower in FSL than FRL animals. Repeated topiramate treatment selectively normalized NPY-LI in this region in the FSL animals. In the hypothalamus, galanin-LI was reduced in FSL compared to FRL animals. Topiramate elevated the hypothalamic concentrations of NPY-LI, CRH-LI, and galanin-LI in both strains. Furthermore, topiramate elevated serum leptin but not corticosterone levels. The present findings show that topiramate has distinct effects on abnormal hippocampal levels of NPY, with possible implications for its anticonvulsant and mood-stabilizing effects. Furthermore, stimulating hypothalamic NPY-LI, CRH-LI and galanin-LI as well as serum leptin levels may be associated with the weight loss-inducing effects of topiramate.

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CRF antagonist partially reverses CRF- and stress-induced effects on feeding

Cited by 288 publications

References 12 publications

The effects of the selective serotonin reuptake-inhibitor fluvoxamine on body weight in Zucker rats are mediated by corticotropin-releasing hormone

The effects of the selective serotonin reuptake-inhibitor fluvoxamine on body weight in Zucker rats are mediated by corticotropin-releasing hormone

Corticotropin-releasing hormone (Crh) maps to mouse Chromosome 3

Topiramate Normalizes Hippocampal NPY-LI in Flinders Sensitive Line ‘Depressed’ Rats and Upregulates NPY, Galanin, and CRH-LI in the Hypothalamus: Implications for Mood-Stabilizing and Weight Loss-Inducing Effects

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