Increase of neuropeptide Y-like immunoreactivity in the paraventricular nucleus of fasting rats

Calzà, Laura; Giardino, Luciana; Battistini, N.; Zanni, Massimo; Galetti, Silvia; Protopapa, Francesco; Velardo, A

doi:10.1016/0304-3940(89)90336-4

Cited by 87 publications

(27 citation statements)

References 13 publications

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“…Although subsequent studies have shown that such effects can be produced by injection of NPY also into select other sites, most potently the nearby located perifornical region [14], there is experimental evidence supporting the view that the earlier results were due to de facto effects in the PVH rather than passive spread of the injection to the perifornical region. Thus, similarly to changes observed in the arcuate nucleus, NPY peptide levels in the PVH increase in response to starvation [15, 16]and are elevated in animals with a natural preference for high-carbohydrate diets [17, 18]. Subsequent studies have also extended the range of energy metabolism parameters affected by NPY transmission in the PVH [19], including regulation of pituitary hormone release [20, 21].…”

Section: Introductionmentioning

confidence: 98%

Neuropeptide Y Innervation and Neuropeptide-Y-Y1-Receptor-Expressing Neurons in the Paraventricular Hypothalamic Nucleus of the Mouse

Broberger¹,

Visser²,

Kuhar³

et al. 1999

Neuroendocrinology

108

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The paraventricular hypothalamic nucleus (PVH) serves as integrator and link between the neuroendocrine and autonomic nervous systems. Neuropeptide-Y (NPY)-producing neurons in the arcuate nucleus project to the PVH, where neurons expressing NPY Y1 receptor (Y1R) have been demonstrated. This projection has been suggested to be involved in the regulation of parameters related to energy metabolism, e.g. food intake and thermoregulation. The present study aimed at characterizing this pathway and chemically defining Y1R-expressing neurons by means of immunohistochemistry. The densely distributed NPY-immunoreactive (ir) terminals in the PVH co-stained for agouti gene-related protein (AGRP) mainly in the medial parvocellular regions, indicating an origin in the arcuate nucleus. This was in contrast to noradrenergic/adrenergic terminals in the PVH, which were less frequently seen to contain NPY-like immunoreactivity. Furthermore, AGRP-ir terminals were seen forming abundant close appositions on Y1R-ir cell bodies. Double staining revealed co-existence of Y1R-like immunoreactivity and immunoreactivities for thyrotropin-releasing hormone (TRH) and, to a minor extent, cocaine- and amphetamine-regulated transcript peptide in parvocellular neurons. No Y1R-like immunoreactivity was noted in parvocellular neurons expressing corticotropin-releasing hormone or in magnocellular neurons expressing vasopressin or oxytocin. The present results suggest that the arcuatoparaventricular NPY projection targets the TRH neurons preferentially via the Y1R, whereas the NPYergic regulation of corticotropinergic and magnocellular neurons may be relayed through other subtypes of NPY receptors. This study further defines the link between NPY-induced feeding and the hypothalamus-pituitary-thyroid axis.

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Section: Introductionmentioning

confidence: 98%

Neuropeptide Y Innervation and Neuropeptide-Y-Y1-Receptor-Expressing Neurons in the Paraventricular Hypothalamic Nucleus of the Mouse

Broberger¹,

Visser²,

Kuhar³

et al. 1999

Neuroendocrinology

108

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“…Concentrations of endogenous NPY in some hypotha lamic nuclei were elevated in rats deprived of food for brief periods of time [11,12]. Elevated tissue stores of NPY probably reflected increased synthesis of the pep tide because concentrations of the mRNA which encodes NPY were also increased in the arcuate nucleus of hungry rats [13].…”

mentioning

confidence: 85%

Effect of Growth Retardation on Pituitary Luteinizing Hormone and Hypothalamic Neuropeptide Y in Ovariectomized Sheep

Ober¹,

Malven²

1992

Neuroendocrinology

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The possible role of neuropeptide Y (NPY) in mediating the relationship between pituitary LH secretion and growth retardation due to restricted feeding was examined in ovariectomized (OVX) prepubertal ewe lambs. One specific objective examined whether there was an inverse relationship between concentrations of NPY in four diencephalic brain regions and pituitary LH secretion in ewe lambs 29-30 weeks old which had been growth retarded since 8 weeks and OVX at 24 weeks. Through dietary restriction, body weight was held constant at 20.7 ± 0.5 kg in 13 growth-retarded ewes as compared with 48.0 ± 0.6 kg for 5 age-matched control ewes at 29-30 weeks of age. Episodic LH was quantified at 10-min intervals for 190 min/day on 3 of the 8 days immediately before euthanasia. Serum LH averaged 6.5 ± 0.6 ng/ml in control ewes with a mean pulse frequency of 1.0 ± 0.1 pulses/h. Serum LH in growth-retarded ewes was much less episodic (0.2 ± 0.05 pulses/h) and averaged only 1.2 ± 0.2 ng/ml. All ewes were euthanized during week 30, and the following brain regions were dissected: basal forebrain, preoptic area, median eminence and remainder of hypothalamus. Following extraction, NPY concentrations (pg/mg of original tissue) were quantified by radioimmunoassay. In each brain region, NPY concentrations were greater (p < 0.05) in 6 growth-retarded ewes than in 5 control ewes (median eminence: 5.2 vs. 0.6; remainder of hypothalamus: 3.3 vs. 0.8; preoptic area: 3.1 vs. 0.8, and basal forebrain: 2.2 vs. 1.2). A secondary objective examined whether the LH and NPY parameters were rapidly altered by transient changes in feed consumption. Therefore, a subgroup of 7 growth-retarded ewes was given access to increased feed during the last week of the experiment (denoted as refed growth-retarded), but feed consumption and weight gain were highly variable as only 1 ewe maintained her initially increased feed consumption for the entire 7 days. Secretion of LH as reflected in mean concentrations (2.1 ± 0.5 ng/ml) and pulse frequency (0.4 ± 0.1 pulses/h) was slightly increased (p < 0.05) in refed ewes. However, NPY concentrations (median eminence: 6.6; remainder of hypothalamus: 3.6; preoptic area: 3.6, and basal forebrain: 2.5) in the 7 refed growth-retarded ewes were similar to those of the 6 growth-retarded ewes which were not refed. Among individual refed growth-retarded ewes, there was no clear relationship among weight gain/feed consumption and hypothalamic NPY. In summary, steroid-independent suppression of LH secretion in chronically growth-retarded ewes was inversely related to elevated levels of NPY in median eminence and other diencephalic regions. Increased food availability forpnly 7 days reversed only slightly the suppression of LH and did not affect the elevated levels of hypothalamic NPY. Except for these divergent changes in refed ewes, the main results of this study are consistent with the hypothesis that increased neural production of NPY contributed to suppression of LH release in growth-retarded OVX ewes.

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“…Also, NPY and CCK con centrations in specific brain areas are altered by feeding and fasting, respectively (13,17). Moreover, NPY and CCK are known to function as signal mediators, regu lating food intake and the body weight balance in the hypothalamus (14)(15)(16).…”

Section: Discussionmentioning

confidence: 99%

“…In the brain, the actions of NPY for energy homeostasis are exerted mostly within the hypothalamus (12). Increases in both biosynthesis and the release of NPY along the distinct neuronal circuits constitute a specific hypothalamic response to the stim ulation of food intake (13). Therefore, NPY is believed to be a key neurotransmitter in the regulation of food intake and energy homeostasis (14,15).…”

mentioning

confidence: 99%

Expressional Changes of Neuropeptide Y and Cholecystokinin in the Arcuate and Paraventricular Nuclei after Capsaicin Administration

Lee

Nam

Lee

et al. 2004

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryDespite its toxicity, a great deal of attention has been paid to the anorexic effect of capsaicin in the treatment of obesity-related neurotransmitters/neuromodulators . To determine if capsaicin has any effects on the orexigenic or anorexigenic peptides , the neu ropeptide Y (NPY) and cholecystokinin (CCK)-imunoreactivities were demonstrated in the rat hypothalamus by immunohistochemistry after capsaicin administration . There was a significantly lower concentration of NPY immunopositive cells in the arcuate and paraventricular nuclei of the capsaicin treated rats. In contrast, the CCK expressions level was higher in the paraventricular nucleus of the capsaicin treated rats than in the control rats. These results suggest that capsaicin influence neuropeptides such as orexigenic NPY and anorexigenic CCK related to control food intake.

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Increase of neuropeptide Y-like immunoreactivity in the paraventricular nucleus of fasting rats

Cited by 87 publications

References 13 publications

Neuropeptide Y Innervation and Neuropeptide-Y-Y1-Receptor-Expressing Neurons in the Paraventricular Hypothalamic Nucleus of the Mouse

Neuropeptide Y Innervation and Neuropeptide-Y-Y1-Receptor-Expressing Neurons in the Paraventricular Hypothalamic Nucleus of the Mouse

Effect of Growth Retardation on Pituitary Luteinizing Hormone and Hypothalamic Neuropeptide Y in Ovariectomized Sheep

Expressional Changes of Neuropeptide Y and Cholecystokinin in the Arcuate and Paraventricular Nuclei after Capsaicin Administration

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