Neuropeptide Y Receptor Gene y6: Multiple Deaths or Resurrections?

Starbäck, Paula; Wraith, Amanda; Eriksson, Henrik; Larhammar, Dan

doi:10.1006/bbrc.2000.3656

Cited by 64 publications

(35 citation statements)

References 18 publications

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“…Thus PP and Y3 receptors were excluded from the present study carried out with 125 I-pPYY as a radioligand. The Y6 receptor is a pseudogene in mouse and is absent in rat as well as in human (Starback et al, 2000). Conversely, the Y1, Y2, and Y5 receptors from the different species show similar affinities for NPY and PYY peptides and could thus be labeled with the radioactive probe 125 IpPYY used in this study.…”

Section: Methodological Considerationsmentioning

confidence: 99%

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Localization and characterization of NPY/PYY receptors in rat frontoparietal cortex during development

Leroux¹

2001

J of Comparative Neurology

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Neuropeptide Y (NPY) is present in most cerebrocortical areas during fetal and postnatal development. In the rat frontal cortex, a dense radial fiber network containing NPY immunoreactivity is observed transiently as early as embryonic day 17 (E17) and disappears at the end of the first postnatal week. We have investigated the distribution of NPY receptors in the frontoparietal cortex at 13 stages of development, from E15 fetuses to adults, by in vitro autoradiography, using (125)I-pPYY as a radioligand. Quantitative receptor density was measured through all cortical layers at each developmental stage. Pharmacological identification of (125)I-pPPY binding sites was made by competition experiments using pNPY or [Leu(31),Pro(34)]pNPY and pNPY(13-36), as selective competitors for Y1 and Y2 receptors, respectively. NPY receptors were first detected in the cerebral cortex at low densities at E19 in a thin layer of tissue corresponding to the inner half of the intermediate zone (IZ) and the upper ventricular zone (VZ). The neuroepithelium did not contain binding sites. High densities of sites were observed by E21 onward to P10 in the deep cortical layers corresponding to the IZ and layers V-VI. A decreasing gradient of receptor density was observed from layer VI to the marginal zone (layer I). The distribution of NPY receptors does not match with the perikarya of transient NPY-immunoreactive neurons located in the cortical plate but does coincide with their axonal extension. The receptor density decreased abruptly between P10 and P12 in deep layers, whereas a moderate expression of binding sites is detected from P10 to P12 in layers I-III. By P14, the binding level was the lowest observed in the postnatal period. From P21 onward, receptors were observed in superficial layers I-III, and their density rose by two- to threefold up to adulthood. Competition studies indicated that the NPY receptors located in the deep cortical layers of the E21 or P1 rat cortex exhibit Y2 receptor type characteristics. The binding sites detected in the superficial layers from P10 to P12 rats also show Y2 receptors characteristics, unlike the NPY receptors in layers II-III of the adult, which behave like Y1 receptors. These data show that different NPY receptor types are successively expressed in specific layers during late gestation and early postnatal life in the rat frontoparietal cortex.

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Section: Methodological Considerationsmentioning

confidence: 99%

“…This receptor, which has not yet been cloned, is unlikely to be present in the rat neocortex (Lee and Miller, 1998). mRNA coding for Y4/PP1, PP2, and Y5 receptors are not expressed in the adult neocortex (Dumont et al, 1998;Parker and Herzog, 1999), and Y6 is absent in the rat (Starback et al, 2000).…”

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confidence: 86%

Localization and characterization of NPY/PYY receptors in rat frontoparietal cortex during development

Leroux¹

2001

J of Comparative Neurology

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“…The Y3 binding and response profiles observed in vivo and ex vivo still remain to be accounted for in molecular terms. Also the Y6 gene is missing from the rat genome and is a pseudogene in several other mammals [65]. As will be discussed below, the redundancy of the Y6 subtype appears to be confined to the mammalian lineage.…”

Section: Vertebrate Y Receptorsmentioning

confidence: 99%

“…All mammals have the genes for the Y1, Y2, Y4 and Y5 subtypes [41,67], while the Y6 gene has been lost or has been rendered non-functional due to mutation in certain mammalian species [65]. The species in which a functional Y6 subtype is missing are spread throughout the mammalian clade.…”

Section: Vertebrate Y Receptorsmentioning

confidence: 99%

“…The species in which a functional Y6 subtype is missing are spread throughout the mammalian clade. Surprisingly, the loss of function seems to be due to distinct mutations in primates [70][71][72], pig [68], and guinea pig [65] while the rat lacks the gene altogether [73]. This suggests that the gene most likely lost importance in the mammalian ancestor and because of this redundancy became prone to mutation.…”

Section: Vertebrate Y Receptorsmentioning

confidence: 99%

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Evolutionary perspective on the NPY-PYY-PP peptides and their receptors

Larhammar

Salaneck

The NPY Family of Peptides in Immune Disorders, Inflammation, Angiogenesis and Cancer

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Neuropeptides in Cancer: Friend and Foe?

Berisha

Borniger

2022

Advanced Biology

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highly dynamic network of various cell types (e.g., cancer cells, endothelial cells, immune cells, fibroblasts) that exert differential effects on neuronal activity within the local environment. Thus, complex signaling between cancer and stromal cells in the TME results in altered firing rates of local nerves. Reciprocally, increased neuronal activity and subsequent release of classical neurotransmitters and/or neuropeptides within the TME results in enhanced cancer progression and subsequent metastasis in various preclinical models and clinical studies. [5][6][7][8][9] Nerves interact with multiple stromal cells in the TME where they indirectly promote tumor growth, progression, and subsequent metastasis. [10] Several studies have demonstrated that sympathetic nerve innervation and subsequent release of the neurotransmitter norepinephrine (NE) is increased in breast tumors. [6,8,9] However, recent work has demonstrated that there is an inverse relationship between tumor weight and norepinephrine content (i.e., larger the size of the tumor, the lower the levels of NE), despite increased innervation of sympathetic nerves within the TME. [11] These findings may be attributed to a relatively unexplored phenomenon: neuropeptide release within the TME. Neuropeptides are molecular messengers that regulate a variety of functions in the central and peripheral nervous systems via binding G-protein-coupled receptors (GPCRs) on target cells. One of the many functions of neuropeptides is serving as growth factors for normal cells via the activation of the heterotrimeric G protein Gq and subsequent synthesis of second messengers and engagement of tyrosine phosphorylation cascades. Neuropeptides act as neuromodulators, in that they can alter the response of neurons to neurotransmitters and other circulating signals, such as leptin, ghrelin, glucose, and insulin-all of which are affected during cancer progression. [12][13][14][15][16][17] For example, both neuropeptide Y (NPY) and hypocretin/orexin neurons appear to mediate some of the orexigenic effects of centrally administered ghrelin as administration of NPY receptor antagonists attenuated ghrelininduced feeding. Similarly, ghrelin-induced feeding was suppressed in orexin knockout mice, indicating that ghrelin may stimulate feeding through both the orexin and NPY systems. [18] However, neuropeptide signaling is exploited within cancer cells and many studies demonstrate the contribution of neuropeptides in tumor cell proliferation and migration, [19] with many major neuropeptides also potentially contributing to cancer processes (see Table 1). Additionally, neuropeptides exert direct Neuropeptides are small regulatory molecules found throughout the body, most notably in the nervous, cardiovascular, and gastrointestinal systems. They serve as neurotransmitters or hormones in the regulation of diverse physiological processes. Cancer cells escape normal growth control mechanisms by altering their expression of growth factors, receptors, or intracellular signals, and neuropeptid...

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Neuropeptide Y Receptor Gene y6: Multiple Deaths or Resurrections?

Cited by 64 publications

References 18 publications

Localization and characterization of NPY/PYY receptors in rat frontoparietal cortex during development

Localization and characterization of NPY/PYY receptors in rat frontoparietal cortex during development

Evolutionary perspective on the NPY-PYY-PP peptides and their receptors

Neuropeptides in Cancer: Friend and Foe?

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