Reduced hypophagic effects of d-fenfluramine and the 5-HT2C receptor agonist mCPP in 5-HT1B receptor knockout mice

Lee, Michelle D.; Somerville, Elizabeth M.; Kennett, Guy A.; Dourish, C T; Clifton, Peter G.

doi:10.1007/s00213-004-1864-0

Cited by 56 publications

(35 citation statements)

References 33 publications

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“…However, other studies have also failed to find a significant hypophagic effect of this dose, even under non-food-deprived conditions, and have only reported non-specific effects of a 10 mg/kg dose (e.g. Lee et al 2004). The discrepancy between the effects of fenfluramine on food intake and on BSS measurements may be explained by the use of a time sampling method of observation in the present study.…”

Section: Discussioncontrasting

confidence: 68%

Mice overexpressing the 5-hydroxytryptamine transporter show no alterations in feeding behaviour and increased non-feeding responses to fenfluramine

et al. 2008

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Section: Discussioncontrasting

confidence: 68%

Mice overexpressing the 5-hydroxytryptamine transporter show no alterations in feeding behaviour and increased non-feeding responses to fenfluramine

et al. 2008

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“…As reported previously, d-fenfluramine induced Fos-like immunoreactivity in a dose-dependent manner in many brain regions associated with energy homeostasis (Heisler et al, 2002), including the arcuate and paraventricular nuclei of the hypothalamus. These hypothalamic regions are proposed targets for d-fenfluramine anorexia because they receive direct input from 5-HT dorsal raphe nucleus (DRN) neurons (Heisler et al, 2002) and because hypothalamic 5-HT 2C receptors are thought to mediate the hypophagic effects of d-fenfluramine in mice (Hewitt et al, 2002;Lee et al, 2004). The DRN contains a high density of CRFR2 and lower levels of CRFR1 and receives CRF projections from a variety of forebrain and limbic structures, including the amygdala and BNST.…”

Section: Discussionmentioning

confidence: 99%

Urocortin 2-Deficient Mice Exhibit Gender-Specific Alterations in Circadian Hypothalamus–Pituitary–Adrenal Axis and Depressive-Like Behavior

Chen¹,

Zorrilla²,

Smith³

et al. 2006

J. Neurosci.

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Gender differences in hypothalamus-pituitary-adrenal (HPA) axis activation and the prevalence of mood disorders are well documented. Urocortin 2, a recently identified member of the corticotropin-releasing factor family, is expressed in discrete neuroendocrine and stress-related nuclei of the rodent CNS. To determine the physiological role of urocortin 2, mice null for urocortin 2 were generated and HPA axis activity, ingestive, and stress-related behaviors and alterations in expression levels of CRF-related ligands and receptors were examined. Here we report that female, but not male, mice lacking urocortin 2 exhibit a significant increase in the basal daily rhythms of ACTH and corticosterone and a significant decrease in fluid intake and depressive-like behavior. The differential phenotype of urocortin 2 deficiency in female and male mice may imply a role for urocortin 2 in these gender differences.

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“…In another study, however, 5HT-1BR-KO mice displayed increased exploratory behavior but no change in food intake [321]. Serotonin 1BR agonists produce hypophagia, which is attenuated by 1BR antagonist treatment [322,323].…”

Section: Serotoninmentioning

confidence: 90%

Neuroendocrine control of satiation

Asarian¹,

Bächler

2014

Hormone Molecular Biology and Clinical Investigation

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Abstract:Eating is a simple behavior with complex functions. The unconscious neuroendocrine process that stops eating and brings a meal to its end is called satiation. Energy homeostasis is mediated accomplished through the control of meal size via satiation. It involves neural integrations of phasic negative-feedback signals related to ingested food and tonic signals, such as those related to adipose tissue mass. Energy homeostasis is accomplished through adjustments in meal size brought about by changes in these satiation signals. The best understood meal-derived satiation signals arise from gastrointestinal nutrient sensing. Gastrointestinal hormones secreted during the meal, including cholecystokinin, glucagon-like peptide 1, and PYY, mediate most of these. Other physiological signals arise from activation of metabolic-sensing neurons, mainly in the hypothalamus and caudal brainstem. We review both classes of satiation signal and their integration in the brain, including their processing by melanocortin, neuropeptide Y/agouti-related peptide, serotonin, noradrenaline, and oxytocin neurons. Our review is not comprehensive; rather, we discuss only what we consider the best-understood mechanisms of satiation, with a special focus on normally operating physiological mechanisms.

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Reduced hypophagic effects of d-fenfluramine and the 5-HT2C receptor agonist mCPP in 5-HT1B receptor knockout mice

Abstract: The hypophagic effect of d-fenfluramine in mice is unlikely to be mediated by the 5-HT1B receptor. Instead, the evidence suggests that an adaptive change in 5-HT2C receptor function occurs in 5-HT1B receptor KO mice and contributes to their reduced response to d-fenfluramine.

Cited by 56 publications

References 33 publications

Mice overexpressing the 5-hydroxytryptamine transporter show no alterations in feeding behaviour and increased non-feeding responses to fenfluramine

Mice overexpressing the 5-hydroxytryptamine transporter show no alterations in feeding behaviour and increased non-feeding responses to fenfluramine

Urocortin 2-Deficient Mice Exhibit Gender-Specific Alterations in Circadian Hypothalamus–Pituitary–Adrenal Axis and Depressive-Like Behavior

Neuroendocrine control of satiation

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