Prolactin-releasing peptide is a potent mediator of stress responses in the brain through the hypothalamic paraventricular nucleus

Mera, Takashi; Fujihara, Hiroaki; Kawasaki, Makoto; Hashimoto, Hirofumi; Saito, Takeshi; Shibata, Minori; Saito, Jun; Oka, Takahiro; Tsuji, Sadatoshi; Onaka, Tatsushi; Ueta, Yoichi

doi:10.1016/j.neuroscience.2006.04.023

Cited by 33 publications

(35 citation statements)

References 77 publications

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“…Energy homeostasis is regulated by various orexigenic and anorexigenic peptides in the hypothalamus. Administration of PrRP activates CRH neurons in the hypothalamus (37), and PrRP-induced anorexia is attenuated by a CRH receptor antagonist (13). However, in the present study, there was no significant decrease in CRH mRNA expression in the paraventricular nucleus, suggesting that changes in CRH neuronal activity may not be the main cause of obesity in PrRP-deficient mice.…”

Section: Discussioncontrasting

confidence: 81%

“…Animals were injected i.c.v. with anti-PrRP mAb (2 μl [mice] or 8 μl [rats]; 4.9 mg/ml P2L-1C; Takeda Pharmaceutical Co.) (8,19,26,37) or control IgG (4.9 mg/ml mouse IgG; Sigma-Aldrich) via inner cannulae (32-gauge [mice] or 30-gauge [rats]). Permission of Takeda Chemical Industries Ltd. is necessary for the distribution of antiPrRP mAb (P2L-1C).…”

Section: Surgery and Icv Injection Of An Anti-prrp Mabmentioning

confidence: 99%

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Endogenous prolactin-releasing peptide regulates food intake in rodents

Matsumoto²,

et al. 2008

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Food intake is regulated by a network of signals that emanate from the gut and the brainstem. The peripheral satiety signal cholecystokinin is released from the gut following food intake and acts on fibers of the vagus nerve, which project to the brainstem and activate neurons that modulate both gastrointestinal function and appetite. In this study, we found that neurons in the nucleus tractus solitarii of the brainstem that express prolactin-releasing peptide (PrRP) are activated rapidly by food ingestion. To further examine the role of this peptide in the control of food intake and energy metabolism, we generated PrRP-deficient mice and found that they displayed late-onset obesity and adiposity, phenotypes that reflected an increase in meal size, hyperphagia, and attenuated responses to the anorexigenic signals cholecystokinin and leptin. Hypothalamic expression of 6 other appetite-regulating peptides remained unchanged in the PrRP-deficient mice. Blockade of endogenous PrRP signaling in WT rats by central injection of PrRP-specific mAb resulted in an increase in food intake, as reflected by an increase in meal size. These data suggest that PrRP relays satiety signals within the brain and that selective disturbance of this system can result in obesity and associated metabolic disorders.

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Section: Discussioncontrasting

confidence: 81%

Section: Surgery and Icv Injection Of An Anti-prrp Mabmentioning

confidence: 99%

Endogenous prolactin-releasing peptide regulates food intake in rodents

Matsumoto²,

et al. 2008

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“…Thus, adaptive neuroendocrine and behavioral anxiety responses to visceral stressors are contingent upon signaling between afferent sensory inputs, the cNTS, and the forebrain, while visceral stress-induced hypophagia can be mediated by cNTS projections to local brainstem circuits (Figure 3). Numerous studies report that cNTS NA, PrRP, and GLP-1 neurons are activated by a broad array of visceral stressors, including: hemorrhage (Morales and Sawchenko 2003; Uchida et al 2010), supraphysiological systemic doses of CCK (Rinaman 1999b; Lawrence et al 2002; Maniscalco and Rinaman 2013), lipopolysaccharide (LPS) (Mera et al 2006), LiCl (Rinaman 1999a), and interleukin-1 (Li et al 1996; Sawchenko et al 2000). …”

Section: The Role Of the Cnts In Central Stress Integrationmentioning

confidence: 99%

Interoceptive modulation of neuroendocrine, emotional, and hypophagic responses to stress

Maniscalco

Rinaman

2017

Physiology & Behavior

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Periods of caloric deficit substantially attenuate many centrally mediated responses to acute stress, including neural drive to the hypothalamic-pituitary-adrenal (HPA) axis, anxiety-like behavior, and stress-induced suppression of food intake (i.e., stress hypophagia). It is posited that this stress response plasticity supports food foraging and promotes intake during periods of negative energy balance, even in the face of other internal or external threats, thereby increasing the likelihood that energy stores are repleted. The mechanisms by which caloric deficit alters central stress responses, however, remain unclear. The caudal brainstem contains two distinct populations of stress-recruited neurons [i.e., noradrenergic neurons of the A2 cell group that co-express prolactin-releasing peptide (PrRP+ A2 neurons), and glucagon-like peptide 1 (GLP-1) neurons] that also are responsive to interoceptive feedback about feeding and metabolic status. A2/PrRP and GLP-1 neurons have been implicated anatomically and functionally in the central control of the HPA axis, anxiety-like behavior, and stress hypophagia. The current review summarizes a growing body of evidence that caloric deficits attenuate physiological and behavioral responses to acute stress as a consequence of reduced recruitment of PrRP+ A2 and hindbrain GLP-1 neurons, accompanied by reduced signaling to their brainstem, hypothalamic, and limbic forebrain targets.

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“…The medullary neurons are also activated by nociceptive stimuli including foot shock (Morales & Sawchenko 2003). Furthermore, the expression of PrRP mRNA in the NTS and VLM is up-regulated by restraint stress or formalin injection (Mera et al 2006). Like PrRP, stressful stimuli evoke increases in blood pressure and alter feeding behaviour, making it tempting to speculate that PrRP neurons may regulate feeding in times of stress.…”

Section: Prrp Familymentioning

confidence: 99%

The role of RFamide peptides in feeding

Bechtold

Luckman

2007

Journal of Endocrinology

113

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In the three decades since FMRFamide was isolated from the clam Macrocallista nimbosa, the list of RFamide peptides has been steadily growing. These peptides occur widely across the animal kingdom, including five groups of RFamide peptides identified in mammals. Although there is tremendous diversity in structure and biological activity in the RFamides, the involvement of these peptides in the regulation of energy balance and feeding behaviour appears consistently through evolution. Even so, questions remain as to whether feedingrelated actions represent a primary function of the RFamides, especially within mammals. However, as we will discuss here, the study of RFamide function is rapidly expanding and with it so is our understanding of how these peptides can influence food intake directly as well as related aspects of feeding behaviour and energy expenditure.

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Prolactin-releasing peptide is a potent mediator of stress responses in the brain through the hypothalamic paraventricular nucleus

Cited by 33 publications

References 77 publications

Endogenous prolactin-releasing peptide regulates food intake in rodents

Endogenous prolactin-releasing peptide regulates food intake in rodents

Interoceptive modulation of neuroendocrine, emotional, and hypophagic responses to stress

The role of RFamide peptides in feeding

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