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Short-term depletion of nicotinic acetylcholine receptor subunits in Drosophila enterocytes

ABSTRACT: Bulk RNAseq from whole Drosophila melanogaster guts expressing either mCherry-RNAi (control) or RNAi against nicotinic acetylcholine receptor subunits β1 and β3 (nAchRβ1 and nAchRβ3) under control of a enterocyte-specific driver to assess their role in barrier function.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE236069 | GEO | 2023/08/23

REPOSITORIES: GEO

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whole brains from nicotinic acetylcholine receptor subunit mutant mice and littermate controls

Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Keywords: knockout mice, nicotinic acetylcholine receptor

2006-09-22 | GSE5320 | GEO

Drosophila nicotinic acetylcholine receptor subunits and their native interactions with insecticidal peptide toxins

Project description:Description Drosophila melanogaster nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels that present a target for insecticides. However, a better understanding of in vioreceptor subunit composition is needed for effective design of insecticides. Alpha-neurotxins are known as peptide toxins capable to block nAChRs by binding to its target subunits. To facilitate the analysis of nAChRs we used a CRISPR/Cas9 strategy to generate null alleles for all ten nAChR subunit genes. We studied interactions of nAChRs to a snake toxin by using styrene maleic acid lipid particles (SMALPs) extraction method. For the null alleles which are impaired in locomotor activities we examined the binding of nAChRs incorporated into SMALPs to alpha bungarotoxin by employing mass spectrometry. We show native ligand interactions to Dalpha5, Dalpha6 and Dalpha7 subunits and reveal glycosylation sites of Dalpha5 and Dalpha7 by a glycoproteomic approach. Finally, we report the localization of fluorescent tagged Dalpha6 across nervous system development

2021-10-11 | PXD028484 | Pride

Short-term depletion of acetylcholine synthesis in Drosophila enteroendocrine cells

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RNA sequencing data describing transcriptional changes in aorta of ApoE-/- mice after alpha 7 nicotinic acetylcholine receptor (α7nAChR) stimulation.

Project description:This manuscript is a companion paper to Ulleryd M.U. et al (1). Data shown here include RNA sequencing data from whole aorta of ApoE-/- mice treated with the alpha 7 nicotinic acetylcholine receptor (α7nAChR) agonist AZ6983 for 8 weeks using subcutaneously implanted osmotic minipumps. 1. Ulleryd MA, Mjornstedt F, Panagaki D, Yang LJ, Engevall K, Gutierrez S, et al. Stimulation of alpha 7 nicotinic acetylcholine receptor (α7nAChR) inhibits atherosclerosis via immunomodulatory effects on myeloid cells Re-submitted. 2019.

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α7 nicotinic acetylcholine receptor signaling modulates the inflammatory phenotype of fetal brain microglia: first evidence of interference by iron homeostasis.

Project description:We sequenced mRNA from 7 microglia extracted from sheep fetuses exposed to LPS, agonist and antagonist of α7 nicotinic acetylcholine receptor to determine signaling pathway through modeling of α7 during inflammation.

2017-08-11 | GSE101857 | GEO

Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

Project description:Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

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α7 Nicotinic Acetylcholine Receptor Regulates Macrophage-Mediated Neuroinflammation in Dry Eye Disease

Project description:Patients with dry eye disease (DED) often exhibit neurological abnormalities and may even suffer from neuropathic pain and pain-related anxiety or depression. However, addressing nerve abnormalities in DED remains a formidable challenge, as current therapies fail to halt disease progression. Our study found that activating α-7 nicotinic acetylcholine receptor (α7nAChR), a pivotal regulator in the anti-inflammatory pathway connecting the nervous and immune systems, effectively restores corneal epithelium integrity and enhances nerve sensitivity in DED, pointing to its promising therapeutic potential. Furthermore, we have revealed that α7nAChR stimulates genes involved in immune-mediated inflammatory progression and neuroregulation, inhibits the expression of transient receptor potential vanilloid-1 (TRPV1), reinstates corneal nerve density, and alleviates anxiety-like behaviors associated with severe DED by downregulating the proportion of CD86+ M1 macrophages (pro-inflammatory phenotypes). In summary, our findings underscore the activation of α7nAChR as a pioneering therapeutic approach for preserving corneal nerves balance and controlling inflammation in DED.

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Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

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Transcription profiling of brains from wild type and beta4 nicotinic acetylcholine receptor (nAChR) subunit deficient mice to identify genes that might be related to beta4-containing nAChRs activity

Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Experiment Overall Design: The experimental groups included six wild-type mice and five beta4-/- mice. All mice were 6-9 weeks old. Total RNA was extracted from whole brain tissue of the mice.

2007-11-27 | E-GEOD-5320 | biostudies-arrayexpress

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2019-04-29 | GSE123713 | GEO

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