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Y5 Receptors (y5 + receptor)

Distribution by Scientific Domains
Life Sciences100%

Terms modified by Y5 Receptors

  • y5 receptor antagonist
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    Selected Abstracts

    Blockade of the NPY Y5 receptor potentiates circadian responses to light: complementary in vivo and in vitro studies

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2004
    P. C. Yannielli
    Abstract Neuropeptide Y (NPY) is delivered to the suprachiasmatic nuclei (SCN) circadian pacemaker via an input from the thalamic intergeniculate leaflet. NPY can inhibit light-induced responses of the circadian system of Syrian hamsters. Here we studied whether an antagonist to NPY receptors can be used to potentiate photic phase shifts late in the subjective night. First we determined by in situ hybridization that both NPY Y1 and Y5 receptor mRNA are expressed in the SCN of Syrian hamsters. Second, similar to our previous findings at Zeitgeber time 14 (ZT 14, where ZT 12 was the time of lights off), we found that NPY applied at ZT 18.5 onto the SCN region of brain slices maintained in vitro could block NMDA-induced phase advances of the spontaneous firing rate rhythm, and this blocking effect was probably mediated by the Y5 receptor, since co-application of Y5 receptor antagonists completely reversed the effect of NPY, while application of a Y1 receptor antagonist had no effect under the same conditions. Third, we found that co-treatment with a Y5 receptor antagonist in vivo (s.c., 10 mg/kg) not only reversed the effect of NPY applied to the SCN in vivo through a cannula but also significantly potentiated the light-induced phase advance in the absence of NPY. This is the first report of a NPY receptor antagonist having such an effect, and indicates that NPY Y5 receptor antagonists could be clinically useful for potentiating circadian system responses to light. [source]

    Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y2 receptors

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2007
    Margaret J. Morris
    Abstract Neuropeptide Y (NPY) potently suppresses absence seizures in a model of genetic generalized epilepsy, genetic absence epilepsy rats of Strasbourg (GAERS). Here we investigated the Y-receptor subtype(s) on which NPY exerts this anti-absence effect. A dual in vivo approach was used: the cumulative duration of seizures was quantified in adult male GAERS in 90-min electroencephalogram recordings following intracerebroventricular (i.c.v.) injection of: (i) subtype-selective agonists of Y1 ([Leu31Pro34]NPY, 2.5 nmol), Y2 (Ac[Leu28,31]NPY24,36, 3 nmol), Y5 receptors [hPP1,17,Ala31,Aib32]NPY, 4 nmol), NPY (3 nmol) or vehicle; and following (ii) i.c.v. injection of antagonists of Y1 (BIBP3226, 20 nmol), Y2 (BIIE0246, 20 nmol) and Y5 (NPY5RA972, 20 nmol) receptors or vehicle, followed by NPY (3 nmol). Injection of the Y1 - and Y5 -selective agonists resulted in significantly less mean seizure suppression (37.4% and 53.9%, respectively) than NPY (83.2%; P < 0.05), while the Y2 agonist had similar effects to NPY (62.3% suppression, P = 0.57). Food intake was not increased following injection of the Y2 agonist, while significant increases in food intake were seen following NPY and the other Y-subtype agonists. Compared with vehicle, NPY injection suppressed seizures following the Y1 and Y5 antagonists (45.3% and 80.1%, respectively, P < 0.05), but not following the Y2 antagonist (5.1% suppression, P = 0.46). We conclude that NPY Y2 receptors are more important than Y1 and Y5 receptors in mediating the effect of NPY to suppress absence seizures in a genetic rat model. Y2 receptor agonists may represent targets for novel drugs against genetic generalized epilepsies without resulting in appetite stimulation. [source]

    Neuropeptide Y inhibits [Ca2+]i changes in rat retinal neurons through NPY Y1, Y4, and Y5 receptors

    JOURNAL OF NEUROCHEMISTRY, Issue 5 2009
    Ana Rita Álvaro
    Abstract Neuropeptide Y (NPY) and NPY receptors are widely distributed in the CNS, including the retina, but the role of NPY in the retina is largely unknown. The aim of this study was to investigate whether NPY modulates intracellular calcium concentration ([Ca2+]i) changes in retinal neurons and identify the NPY receptors involved. As NPY decreased the [Ca2+]i amplitudes evoked by 30 mM KCl in only 50% of neurons analyzed, we divided them in two populations: NPY-non-responsive neurons (,2/,1 , 0.80) and NPY-responsive neurons (,2/,1 < 0.80), being the ,2/,1 the ratio between the amplitude of [Ca2+]i increase evoked by the second (,2) and the first (,1) stimuli of KCl. The NPY Y1/Y5, Y4, and Y5 receptor agonists (100 nM), but not the Y2 receptor agonist (300 nM), inhibited the [Ca2+]i increase induced by KCl. In addition, the inhibitory effect of NPY on evoked-[Ca2+]i changes was reduced in the presence of the Y1 or the Y5 receptor antagonists. In conclusion, NPY inhibits KCl-evoked [Ca2+]i increase in retinal neurons through the activation of NPY Y1, Y4, and Y5 receptors. This effect may be viewed as a potential neuroprotective mechanism of NPY against retinal neurodegeneration. [source]

    Neuropeptide Y stimulates retinal neural cell proliferation , involvement of nitric oxide

    JOURNAL OF NEUROCHEMISTRY, Issue 6 2008
    Ana Rita Álvaro
    Abstract Neuropeptide Y (NPY) is a 36 amino acid peptide widely present in the CNS, including the retina. Previous studies have demonstrated that NPY promotes cell proliferation of rat post-natal hippocampal and olfactory epithelium precursor cells. The aim of this work was to investigate the role of NPY on cell proliferation of rat retinal neural cells. For this purpose, primary retinal cell cultures expressing NPY, and NPY Y1, Y2, Y4 and Y5 receptors [Álvaro et al., (2007) Neurochem. Int., 50, 757] were used. NPY (10,1000 nM) stimulated cell proliferation through the activation of NPY Y1, Y2 and Y5 receptors. NPY also increased the number of proliferating neuronal progenitor cells (BrdU+/nestin+ cells). The intracellular mechanisms coupled to NPY receptors activation that mediate the increase in cell proliferation were also investigated. The stimulatory effect of NPY on cell proliferation was reduced by l -nitroarginine-methyl-esther (l -NAME; 500 ,M), a nitric oxide synthase inhibitor, 1H-[1,2,4]oxadiazolo-[4, 3-a]quinoxalin-1-one (ODQ; 20 ,M), a soluble guanylyl cyclase inhibitor or U0126 (1 ,M), an inhibitor of the extracellular signal-regulated kinase 1/2 (ERK 1/2). In conclusion, NPY stimulates retinal neural cell proliferation, and this effect is mediated through nitric oxide,cyclic GMP and ERK 1/2 pathways. [source]