Disinhibition of female sexual behavior by a CRH receptor antagonist in Syrian hamsters

Jones, Juli E.; Pick, Rebecca R.; Davenport, Matthew D.; Keene, Alex C.; Corp, Eric S.; Wade, George N.

doi:10.1152/ajpregu.00233.2002

Cited by 29 publications

(31 citation statements)

References 37 publications

(57 reference statements)

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“…We found that ICV treatment with doses of CRH or urocortin 1 that inhibited sexual receptivity in hamsters also activated the HPA axis. However, restraint stress, which also activated the HPA axis, had no effect at all on hamster estrous behavior (114).…”

Section: What About Stress?mentioning

confidence: 85%

“…Furthermore, astressin rapidly (Ͻ30 min) reverses the established inhibition of sexual receptivity by food deprivation ( Fig. 13) (114). Thus the peptides seem to act far too quickly to depend on changes in steroid receptor levels.…”

Section: Control Of Estrous Behaviormentioning

confidence: 93%

“…ICV infusion of urocortins 1, 2, and 3 inhibit estrous behavior in hamsters, just as CRH does (114,222). Urocortins 2 and 3 are selective for the CRHR2 (136,180), indicating that activation of this receptor alone is sufficient to inhibit receptivity.…”

Section: Control Of Estrous Behaviormentioning

confidence: 96%

“…However, regardless of any possible effects on ERIR, these neurotransmitters almost certainly affect behavior by other mechanisms, too. Estrous behavior responds slowly to decreased fuel oxidation, taking at least 36 h to develop (113), but NPY, CRH, and the urocortins take Ͻ30 min to work (43,114,222). Furthermore, astressin rapidly (Ͻ30 min) reverses the established inhibition of sexual receptivity by food deprivation ( Fig.…”

Section: Control Of Estrous Behaviormentioning

confidence: 99%

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Neuroendocrinology of nutritional infertility

Wade¹,

Jones²

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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228

166

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Natural selection has linked the physiological controls of energy balance and fertility such that reproduction is deferred during lean times, particularly in female mammals. In this way, an energetically costly process is confined to periods when sufficient food is available to support pregnancy and lactation. Even in the face of abundance, nutritional infertility ensues if energy intake fails to keep pace with expenditure. A working hypothesis is proposed in which any activity or condition that limits the availability of oxidizable fuels (e.g., undereating, excessive energy expenditure, diabetes mellitus) can inhibit both gonadotropin-releasing hormone (GnRH)/luteinizing hormone secretion and female copulatory behaviors. Decreases in metabolic fuel availability appear to be detected by cells in the caudal hindbrain. Hindbrain neurons producing neuropeptide Y (NPY) and catecholamines (CA) then project to the forebrain where they contact GnRH neurons both directly and also indirectly via corticotropin-releasing hormone (CRH) neurons to inhibit GnRH secretion. In the case of estrous behavior, the best available evidence suggests that the inhibitory NPY/CA system acts primarily via CRH or urocortin projections to various forebrain loci that control sexual receptivity. Disruption of these signaling processes allows normal reproduction to proceed in the face of energetic deficits, indicating that the circuitry responds to energy deficits and that no signal is necessary to indicate that there is an adequate energy supply. While there is a large body of evidence to support this hypothesis, the data do not exclude nutritional inhibition of reproduction by other pathways and processes, and the full story will undoubtedly be more complex than this. luteinizing hormone; estrous behavior; corticotropin-releasing hormone; neuropeptide Y; hindbrain OF NECESSITY, the physiological controls of reproduction and energy balance are closely intertwined. Living creatures require a steady stream of oxidizable substrates to fuel their many energy-consuming activities, including reproduction. But in nature, energetic demands and opportunities for meal taking can be erratic and sometimes unpredictable, necessitating the existence of physiological and behavioral strategies to maximize chances of individual survival and permit propagation of the species (21,22,200,208).A need to eat constantly is obviated by the presence of internal caloric buffers that store glycogen and fatty acids and provide sustenance in between meals and during brief fasts. When food is abundant, animals adjust their intakes to meet all demands and keep their storage depots full (or overfull in an increasing number of cases). However, a more likely scenario in nature and during human evolution is that food can be scarce or have a very high acquisition cost. In that case, animals adjust their energetic priorities, i.e., how they partition and use the available metabolic fuels (Fig.

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Section: What About Stress?mentioning

confidence: 85%

Section: Control Of Estrous Behaviormentioning

confidence: 93%

Section: Control Of Estrous Behaviormentioning

confidence: 96%

Section: Control Of Estrous Behaviormentioning

confidence: 99%

See 2 more Smart Citations

Neuroendocrinology of nutritional infertility

Wade¹,

Jones²

2004

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

228

166

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“…Acute stress in rats was shown to result in a short-term hypophagia and a long-term reduction in the rate of weight gain (17). Undernutrition causes inhibition of estrous behavior in female Syrian hamsters, and this was shown to involve activation of CRH receptors as a final step (21). Similar to leptin, insulin conveys adi-posity-related signals to the brain (11,35,38).…”

mentioning

confidence: 99%

Peptides that regulate food intake

Cupples

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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IN THIS ISSUE OF THE JOURNAL are published the first group of papers submitted to the Special Call for Papers on the subject "Peptides that Regulate Food Intake." These nine papers (7a, 32a, 37a, 37b, 41a, 42a, 43a, 46a, 49a) illustrate both the breadth and depth of the subject. They continue the contribution made by papers published in the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology toward understanding of the regulation of food intake and body weight. What are these peptides? How do they act? How do they interact among themselves and with other control systems? These are all important questions addressed by recent publications in this journal and highlighted below.Leptin is secreted by adipocytes and signals fat content to neurons in the arcuate nucleus of the hypothalamus. Leptin inhibits release of the potent orexigens neuropeptide Y (NPY) and agouti-related peptide (AgRP), which are coexpressed in neurons of the arcuate nucleus of the hypothalamus. Leptin also increases release, from adjacent neurons, of anorexigens ␣-melanocyte stimulating hormone (␣-MSH) and cocaine-and amphetamine-regulated transcript (CART), which are also coexpressed (38). Food deprivation increases NPY and AgRP mRNA and decreases that of proopiomelanocortin (POMC) in the arcuate nucleus. These changes are largely reversed 6 h after refeeding (43), but not by leptin infusion or a palatable, noncaloric mash, indicating the importance of other postabsorptive factors (43). Zhang et al. (49) showed in several different fat depots of mice that leptin mRNA content varied directly with adipocyte volume, whereas messages for tumor necrosis factor-␣, insulin receptor, and glucocorticoid receptor were all independent of cell volume. Obesity induced by feeding rodents a high-fat or high-energy diet is associated with leptin resistance; leptin becomes less effective at reducing food intake. The leptin resistance caused by changing from chow to a high-fat diet occurred rapidly and was apparent before any change of body composition could take place (26), suggesting that dietary fat, per se, can induce leptin resistance. Importantly, in rats maintained on chow, leptin sensitivity predicts the development of diet-induced obesity when the animals are subsequently placed on a high-energy diet (24). Rats with the lowest leptin sensitivity become most obese. Changes in circulating leptin can be of varying importance in different models of weight loss. For example, lactating sheep are in negative energy balance despite hyperphagia. Here the reduction of plasma leptin appears to be a primary signal for the hyperphagia (42). In contrast, the weight loss induced by acute stress, although associated with reduced circulating leptin, is unchanged when plasma leptin is clamped high (17). In addition to its effects on food intake, leptin also has significant metabolic actions. With the use of different strains of db/db mice having profound leptin resistance due to absence of the long form of the leptin receptor, it was possi...

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Treatment with CRH‐1 antagonist antalarmin reduces behavioral and endocrine responses to social stressors in marmosets (Callithrix kuhlii)

French

Fite

Jensen

et al. 2007

American J Primatol

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Corticotropin-releasing hormone (CRH) has multiple roles in coordinating the behavioral and endocrine responses to a host of environmental challenges, including social stressors. In the present study we evaluated the role of CRH in mediating responses to a moderate social stressor in Wied's black tufted-eared marmosets (Callithrix kuhlii). Male and female marmosets (n=14) were administered antalarmin (a selective CRH-1 receptor antagonist; 50 microg/kg, p.o.) or vehicle in a blind, counterbalanced, crossover design. One hr after treatment, marmosets were separated from long-term pairmates and then housed alone in a novel enclosure for 7 hr. Behavior was recorded during separation and upon reunion with the partner, and urine samples for cortisol assay collected before, during, and after the intervention. Separation from partners elevated urinary cortisol concentrations over baseline for both conditions, but antalarmin treatment reduced the magnitude of the elevation. Antalarmin also lowered rates of behavioral patterns associated with arousal (alarm and "e-e" vocalizations, object manipulate/chew), but had no effect on contact calls, locomotory activity or alertness. Although most patterns of social behavior upon reunion with the partner were not affected by antalarmin, antalarmin-treated marmosets displayed more sexual behavior (mounts and copulations) upon reunion. These data indicate that antagonism of the CRH-1 receptor acts to reduce the magnitude of both endocrine and behavioral responses to a moderate social stressor without causing any overall reduction in alertness or general activity. This supports the hypothesis that CRH, acting through its type 1 receptor, is involved in coordinating the responses to anxiety-producing events. These results further suggest that the marmoset is a useful model for exploration of the role of CRH in mediating the behavioral and neuroendocrine responses to psychosocial stressors, particularly in the context of heterosexual social relationships.

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Disinhibition of female sexual behavior by a CRH receptor antagonist in Syrian hamsters

Cited by 29 publications

References 37 publications

Neuroendocrinology of nutritional infertility

Neuroendocrinology of nutritional infertility

Peptides that regulate food intake

Treatment with CRH‐1 antagonist antalarmin reduces behavioral and endocrine responses to social stressors in marmosets (Callithrix kuhlii)

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