Expression data from NPY Y1R-deficient osteoblastic cells
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ABSTRACT:
PROVIDER: PRJNA471505 | ENA |
REPOSITORIES: ENA
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Project description:NPY signalling via osteoblastic Y1 receptors has been shown to control bone mass but also contributes significantly to the control of whole-body insulin secretion and glucose homeostasis in mice through the release of novel factor(s) which are different from the previously implicated osteocalcin. We used microarrays to identify novel endocrine factors regulated by Y1 receptors and involved in the regulation of bone mass and whole-body homeostasis.
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Project description:Neuropeptide Y (NPY) is an endogenous modulator of neuronal activity by regulating GABA and glutamate release. Previously, we found that estradiol modulates NPY expression in the hippocampal dentate gyrus. Here we investigated which estrogen receptor type activation is required for the NPY expression. Further, we determined effects of estrogen receptor activation on NPY release. Finally, we determined the contribution of estrogen-mediated remodeling of the GABAergic and glutamatergic network in relation to changes in coupling with NPY in ovariectomized rats. We found that activation of either estrogen receptor type increases NPY expression as well as NPY release in the dentate gyrus. We also found that compared to OVX rats, estrogen replacement increases the likeness of synergistic/antagonistic coupling between the NPY and GABAergic synapse genes while the glutamatergic synapse genes are less likely coupled with NPY. The data together suggest that estrogen plays a critical role in regulation of activity of the NPY system and its coupling to GABAergic and glutamatergic synapses in female rat dentate gyrus. Two-conditions (E = beta-estradiol replacement vs O = oil) experiment. Biological replicates: 4E, 4O.
2014-08-02 | E-GEOD-60013 | biostudies-arrayexpress
Project description:Neuropeptide Y (NPY) is an endogenous modulator of neuronal activity by regulating GABA and glutamate release. Previously, we found that estradiol modulates NPY expression in the hippocampal dentate gyrus. Here we investigated which estrogen receptor type activation is required for the NPY expression. Further, we determined effects of estrogen receptor activation on NPY release. Finally, we determined the contribution of estrogen-mediated remodeling of the GABAergic and glutamatergic network in relation to changes in coupling with NPY in ovariectomized rats. We found that activation of either estrogen receptor type increases NPY expression as well as NPY release in the dentate gyrus. We also found that compared to OVX rats, estrogen replacement increases the likeness of synergistic/antagonistic coupling between the NPY and GABAergic synapse genes while the glutamatergic synapse genes are less likely coupled with NPY. The data together suggest that estrogen plays a critical role in regulation of activity of the NPY system and its coupling to GABAergic and glutamatergic synapses in female rat dentate gyrus.
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2012-09-01 | GSE30774 | GEO
Project description:Neuropeptide Y (NPY) exerts powerful feeding related functions in the hypothalamus. However, NPY is also present in extra-hypothalamic nuclei, however their influence on energy homeostasis is unclear. Here we uncover a previously unknown feeding stimulatory pathway that is activated under conditions of stress in combination with calorie dense food with NPY neurons in the central amygdala (CeA) being responsible for an exacerbated response to a combined stress and high fat diet intervention. CeA NPY neuron specific Npy overexpression mimics the obese phenotype seen in a stress/HFD model, which is prevented by the selective ablation of Npy. Using food intake and energy expenditure (EE) as readout we demonstrate that selective activation of CeA NPY neurons results in increased food intake and a decrease in EE, which requires the presence of NPY. Mechanistically it is the diminished insulin signalling capacity on CeA NPY neurons under stress combined with HFD conditions that leads to the exaggerated development of obesity.
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