NPY neurons express somatostatin receptor subtype 1 in the arcuate nucleus

Fodor, Mariann; Elk, Eef J. Van; Huizinga, Carla T; Prins, Tamara; Waal, Henriëtte A. Delemarre-van de

doi:10.1097/00001756-200501190-00008

Cited by 10 publications

(11 citation statements)

References 16 publications

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“…2003). These results, together with the observation that a fraction of orexigenic NPY neurons in the ARC co‐express sst1 (Fodor et al . 2005) has led to the hypothesis that somatostatin may affect the leptin‐mediated regulation of energy homeostasis.…”

supporting

confidence: 57%

“…2000). In addition, orexigenic NPY‐neurons, which were recently shown to co‐express sst1 (Fodor et al . 2005), project inhibitory collaterals to anorexigenic POMC‐neurons (Cowley et al .…”

Section: Discussionmentioning

confidence: 99%

“…We recently demonstrated that leptin-activated STAT3 and different sst-subtypes, as well as SST14 itself, colocalise in neurons of the rat hypothalamic feeding centres (Stepanyan et al 2003). These results, together with the observation that a fraction of orexigenic NPY neurons in the ARC co-express sst1 (Fodor et al 2005) has led to the hypothesis that somatostatin may affect the leptin-mediated regulation of energy homeostasis.…”

mentioning

confidence: 95%

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Somatostatin, a negative‐regulator of central leptin action in the rat hypothalamus

Stepanyan

Kocharyan²,

Behrens³

et al. 2006

Journal of Neurochemistry

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Leptin-responsive neurons of the hypothalamus constitute a heterogeneous population expressing a vast array of different neuropeptides and neurotransmitters, some of which participate in the regulation of hunger and satiety. Here we report that somatostatin modulates the efficacy of leptin-signalling in the rat hypothalamus. Using a two-pulse paradigm at 30-min intervals, we delivered somatostatin or somatostatin receptor subtype-selective agonists in combination with leptin into the lateral cerebral ventricle of stereotaxically cannulated rats. To monitor the effect of somatostatin on the leptin-signalling pathway, we quantified changes in the leptin-mediated activation of STAT3, the signal transducer and activator of transcription 3. Successive administration of somatostatin and leptin diminished the level of STAT3-phosphorylation and nuclear STAT3 translocation in the ventromedial and dorsomedial hypothalamic nuclei, the lateral hypothalamic area, and the arcuate nucleus by about 40% compared to leptin administration alone. Furthermore, application of subtypeselective somatostatin receptor agonists suggests that the observed reduction in leptin-responsiveness is predominantly mediated by the sst3 receptor-subtype, followed by sst1 and sst2. In addition, the intensity of the negative-regulatory effect of somatostatin on leptin-signalling displayed regional differences for the three receptor-subtypes involved. Addressing the functional consequences of the diminished leptin-signalling, behavioural analyses showed that centrally applied somatostatin counteracts the leptin-mediated suppression of food intake. These results suggest that the pleiotropic effector somatostatin also plays a role in the central regulation of energy homeostasis.

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supporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

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Somatostatin, a negative‐regulator of central leptin action in the rat hypothalamus

Stepanyan

Kocharyan²,

Behrens³

et al. 2006

Journal of Neurochemistry

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“…Our last study on anatomical connections between NPY and somatostatin neurons demonstrated such links in prepubertal lambs on the levels of PEV and ARC nuclei (unpublished). The direct interactions between the somatostatin and NPY in the area of ARC nuclei were found in rats where approximately 7% of NPY perikarya coexpressed the specific receptor for somatostatin -sst1 [42].These data suggest that there is an anatomical basis for interactions between these two groups of cells and that NPY neurons can influence the secretion of GH by influencing hypothalamic somatostatin neurons.…”

Section: Neuropeptide Ymentioning

confidence: 76%

Effects of maternal deprivation on the somatotrophic axis and neuropeptide Y in the hypothalamus and pituitary in female lambs. The histomorphometric study.

Polkowska

Wańkowska²

2010

Folia Histochem Cytobiol.

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Abstract:The effects of maternal deprivation on the somatotrophic axis and neuropeptide Y (NPY) neuronal system in the hypothalamus of female lambs were evaluated. Twelve-week-old lambs were divided into two groups: the control (lambs stayed with mothers) and maternally deprived (MD; lambs separated for 3 days from mothers). The expression of immunoreactive (ir) somatostatin in the neurons of the periventricular nucleus (PEV) and in nerve terminals of the median eminence (ME), growth hormone (GH) in the adenohypophyseal cells and NPY in the neurons of the PEV and arcuate (ARC) nuclei of the hypothalamus using immunohistochemistry followed by the image analysis were estimated. Concentrations of GH in the blood plasma were determined by radioimmunoassay. The expression of ir somatostatin in the PEV and ME, ir NPY in the ARC and PEV, ir GH in adenohypophyseal cells, and blood plasma GH concentrations were greater (p<0.05) in MD than in the control lambs. In conclusion, MD affects the somatotrophic axis by enhancement of GH secretion via restraining of somatostatin output. The simultaneous increase of expression of hypothalamic ir NPY suggests NPY involvement in the regulation of psychoemotional stress through the somatotrophic axis in the female lambs.

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“…The stimulatory action of SRIH on GHRH neuronal activity may be mediated via sst1 because infusion of antisense sst1 oligonucleotides suppresses GH release, while antisense sst2 oligonucleotides have no effect [43]. It should also be noted that a recent report suggests NPY neurons, within the arcuate nucleus of rats, may also be targets of direct SRIH regulation, since a subpopulation of these neurons expresses sst1 [44]. …”

Section: Discussionmentioning

confidence: 99%

Expression Analysis of Hypothalamic and Pituitary Components of the Growth Hormone Axis in Fasted and Streptozotocin-Treated Neuropeptide Y (NPY)-Intact (NPY<sup>+/+</sup>) and NPY-Knockout (NPY<sup> –/–</sup>) Mice

et al. 2005

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In the fasted and the streptozotocin (STZ)-induced diabetic male rat, hypothalamic growth hormone (GH)-releasing hormone (GHRH) mRNA levels, and pulsatile GH release are decreased. These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY^+/+) and NPY-knockout (NPY^–/–) mice by ribonuclease protection assay. In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. Under fed conditions the GH axis of NPY^+/+ and NPY^–/– did not differ. In the NPY^+/+ mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. In the NPY^–/– mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. Fasting resulted in an overall increase in circulating GH, which reached significance in the fasted NPY^–/– mouse. Induction of diabetes in NPY^+/+ mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. Induction of diabetes in NPY^+/+ and NPY^–/– mice, using a multiple, low-dose, STZ paradigm (5 consecutive daily injections of 40 mg/kg), did not alter body weight, hypothalamic neuropeptide expression or pituitary receptor expression, with the exception that sst2 mRNA levels were suppressed and GH levels did rise in the NPY^–/– mouse. These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. In contrast to the rat, fasting clearly did not suppress circulating GH levels in mice, but resulted in an overall rise in mean GH levels, similar to that observed in other mammalian species. The fact that many of the fasting-induced changes in the GH axis were observed in the high-dose STZ-treated mice, but were not observed in the multiple, low-dose paradigm, suggests STZ-mediated modulation of GH axis function is dependent on the severity of the catabolic state and not hyperglycemia.

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NPY neurons express somatostatin receptor subtype 1 in the arcuate nucleus

Cited by 10 publications

References 16 publications

Somatostatin, a negative‐regulator of central leptin action in the rat hypothalamus

Somatostatin, a negative‐regulator of central leptin action in the rat hypothalamus

Effects of maternal deprivation on the somatotrophic axis and neuropeptide Y in the hypothalamus and pituitary in female lambs. The histomorphometric study.

Expression Analysis of Hypothalamic and Pituitary Components of the Growth Hormone Axis in Fasted and Streptozotocin-Treated Neuropeptide Y (NPY)-Intact (NPY<sup>+/+</sup>) and NPY-Knockout (NPY<sup> –/–</sup>) Mice

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