PYY(3–36) induces Fos in the arcuate nucleus and in both catecholaminergic and non-catecholaminergic neurons in the nucleus tractus solitarius of rats

Blevins, James E.; Chelikani, Prasanth; Haver, Alvin C.; Reidelberger, Roger D.

doi:10.1016/j.peptides.2007.11.003

Cited by 57 publications

(33 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Immunohistochemical studies suggest that the Y2 receptor is abundantly expressed in various brain regions, including brain stem areas and structures of the limbic system such as the nucleus accumbens (NAc), the amygdala (Amy), the hypothalamus (Hyp) and the hippocampus (Hpc) (Stanic et al, 2006). Consistent with this receptor distribution, peripheral administration of the Y2 receptor agonist PYY 3-36 in rodents has been show to induce neuronal activation in multiple brain areas, as evidenced by immunohistochemical evaluations of the neuronal early gene product c-Fos (Blevins et al, 2008;Stadlbauer et al, 2013a).…”

Section: Introductionmentioning

confidence: 84%

The Y2 receptor agonist PYY3–36 increases the behavioural response to novelty and acute dopaminergic drug challenge in mice

Stadlbauer

Weber

Langhans

et al. 2013

Int. J. Neuropsychopharm.

View full text Add to dashboard Cite

The gastrointestinal hormone PYY(3-36) is a preferential Y2 neuropeptide Y (NPY) receptor agonist. Recent evidence indicates that PYY(3-36) acts on central dopaminergic pathways, but its influence on dopamine-dependent behaviours remains largely unknown. We therefore explored the effects of peripheral PYY(3-36) treatment on the behavioural responses to novelty and to dopamine-activating drugs in mice. In addition, we examined whether PYY(3-36) administration may activate distinct dopamine and γ-aminobutyric acid (GABA) cell populations in the mesoaccumbal and nigrostriatal pathways. We found that i.p. PYY(3-36) injection led to a dose-dependent increase in novel object exploration. The effective dose of PYY(3-36) (1 μg/100 g body weight) also potentiated the locomotor reaction to the indirect dopamine receptor agonist amphetamine and increased stereotyped climbing/leaning responses following administration of the direct dopamine receptor agonist apomorphine. PYY(3-36) administration did not affect activity of midbrain dopaminergic cells as evaluated by double immuno-enzyme staining of the neuronal early gene product c-Fos with tyrosine hydroxylase. PYY(3-36) did, however, lead to a marked increase in the number of cells co-expressing c-Fos with glutamic acid decarboxylase in the nucleus accumbens and caudate putamen, indicating activation of GABAergic cells in dorsal and ventral striatal areas. Our results support the hypothesis that acute administration of the preferential Y2 receptor agonist PYY(3-36) modulates dopamine-dependent behaviours. These effects do not seem to involve direct activation of midbrain dopamine cells but instead are associated with neuronal activation in the major input areas of the mesoaccumbal and nigrostriatal pathways.

show abstract

Section: Introductionmentioning

confidence: 84%

The Y2 receptor agonist PYY3–36 increases the behavioural response to novelty and acute dopaminergic drug challenge in mice

Stadlbauer

Weber

Langhans

et al. 2013

Int. J. Neuropsychopharm.

View full text Add to dashboard Cite

show abstract

“…Importantly, administration of GLP1 or PYY reduced energy intake in both lean and overweight subjects (22). The hypothalamus and the brainstem are thought to be the most relevant areas of satiating and hypophagic effects of peripheral GLP1 and PYY (23,24).…”

Section: Discussionmentioning

confidence: 99%

Anorexigenic postprandial responses of PYY and GLP1 to slow ice cream consumption: preservation in obese adolescents, but not in obese adults

Rigamonti

Agosti

Compri

et al. 2013

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: Eating slowly increases the postprandial responses of some anorexigenic gut hormones in healthy lean subjects. As the rate of food intake is positively associated with obesity, the aim of the study was to determine whether eating the same meal at different rates evokes different postprandial anorexigenic responses in obese adolescent and adult subjects. Design and methods: Eighteen obese adolescents and adults were enrolled. A test meal was consumed on two different sessions by each subject, meal duration taking either 5 min (fast feeding) or 30 min (slow feeding). Circulating levels of glucagon-like peptide 1 (GLP1), peptide YY (PYY), glucose, insulin, and triglycerides were measured over 210 min. Visual analog scales were used to evaluate the subjective feelings of hunger and satiety. Results: Fast feeding did not stimulate GLP1 release in obese adolescent and adults, whereas slow feeding increased circulating levels of GLP1 only in obese adolescents. Plasma PYY concentrations increased both in obese adolescents and in adults, irrespective of the eating rate, but slow feeding was more effective in stimulating PYY release in obese adolescents than in adults. Simultaneously, slow feeding evoked a higher satiety only in obese adolescents compared with fast feeding but not in obese adults. In obese adolescents, slow feeding decreased hunger (only at 210 min). Irrespective of the eating rate, postprandial responses of insulin and triglycerides were higher in obese adults than in obese adolescents. Conclusion: Slow feeding leads to higher concentrations of anorexigenic gut peptides and favors satiety in obese adolescents, but this physiological control of food intake is lost in obese adults.

show abstract

“…It is well known that NTS catecholaminergic neurons project to the parvocellular subdivision of the PVN; therefore, ascending projections from NTS presumably could activate CRF neurons in the PVN (21). On the other hand, activation of ARC following a meal has been associated with direct actions of meal-related signals, such as GLP-1 and peptide YY (3,23).…”

Section: Discussionmentioning

confidence: 99%

Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses

Uchôa¹,

Sabino²,

Ruginsk³

et al. 2009

Journal of Applied Physiology

View full text Add to dashboard Cite

Uchoa ET, Sabino HA, Ruginsk SG, Antunes-Rodrigues J, Elias LL. Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses. J Appl Physiol 106: 596 -604, 2009. First published November 20, 2008 doi:10.1152/japplphysiol.90865.2008.-Glucocorticoids have major effects on food intake, demonstrated by the decrease of food intake following adrenalectomy. Satiety signals are relayed to the nucleus of the solitary tract (NTS), which has reciprocal projections with the arcuate nucleus (ARC) and paraventricular nucleus (PVN) of the hypothalamus. We evaluated the effects of glucocorticoids on the activation of hypothalamic and NTS neurons induced by food intake in rats subjected to adrenalectomy (ADX) or sham surgery 7 days before the experiments. One-half of ADX animals received corticosterone (ADXϩB) in the drinking water (B: 25 mg/l). Fos/tyrosine hydroxylase (TH), Fos/corticotrophin-releasing factor (CRF) and Fos immunoreactivity were assessed in the NTS, PVN, and ARC, respectively. Food intake and body weight were reduced in the ADX group compared with sham and ADXϩB groups. Fos and Fos/TH in the NTS, Fos, and Fos/CRF immunoreactive neurons in the PVN and Fos in the ARC were increased after refeeding, with higher number in the ADX group, compared with sham and ADXϩB groups. CCK administration showed no hypophagic effect on ADX group despite a similar increase of Fos/TH immunoreactive neurons in the NTS compared with sham and ADXϩB groups, suggesting that CCK alone cannot further increase the anorexigenic effect induced by glucocorticoid deficiency. The present data indicate that glucocorticoid withdrawal reduced food intake, which was associated with higher activation of ARC, CRF neurons of the PVN, and catecholaminergic neurons of the NTS. In the absence of glucocorticoids, satiety signals elicited during a meal lead to an augmented activation of brain stem and hypothalamic pathways. glucocorticoids; food intake; satiety signals; nucleus of the solitary tract; paraventricular nucleus of the hypothalamus; arcuate nucleus of the hypothalamus GLUCOCORTICOIDS PLAY AN IMPORTANT ROLE in the control of feeding behavior. Increased food intake and body weight gain are associated with glucocorticoid treatment in humans (46). On the other hand, bilateral adrenalectomy (ADX) reduces food intake and body weight gain, and these effects are reversed by glucocorticoid replacement in rats (12). Furthermore, ADX reduces hyperphagia and obesity in different experimental models, whereas glucocorticoid replacement reverses these effects (4,8,52). Hypophagia induced by ADX has been associated with a decrease of mRNA expression of hypothalamic neuropeptide Y (NPY), a potent orexigenic neuropeptide (41). ADX also may reduce food intake through the increase of corticotrophin-releasing factor (CRF) mRNA expression in the paraventricular nucleus (PVN), since CRF is a well-known anorexigenic peptide (1, 2). CRF neurons in the PVN receive projections from neurons of the nucleus of the...

show abstract

PYY(3–36) induces Fos in the arcuate nucleus and in both catecholaminergic and non-catecholaminergic neurons in the nucleus tractus solitarius of rats

Cited by 57 publications

References 39 publications

The Y2 receptor agonist PYY3–36 increases the behavioural response to novelty and acute dopaminergic drug challenge in mice

The Y2 receptor agonist PYY3–36 increases the behavioural response to novelty and acute dopaminergic drug challenge in mice

Anorexigenic postprandial responses of PYY and GLP1 to slow ice cream consumption: preservation in obese adolescents, but not in obese adults

Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses

Contact Info

Product

Resources

About