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Last update 23 Jan 2025

CHRNA10

Last update 23 Jan 2025

Basic Info

Synonyms

acetylcholine receptor, nicotinic, alpha 10 (neuronal), cholinergic receptor nicotinic alpha 10 subunit, cholinergic receptor, nicotinic alpha 10

+ [7]

Introduction

Ionotropic receptor with a probable role in the modulation of auditory stimuli. Agonist binding may induce an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane. The channel is permeable to a range of divalent cations including calcium, the influx of which may activate a potassium current which hyperpolarizes the cell membrane. In the ear, this may lead to a reduction in basilar membrane motion, altering the activity of auditory nerve fibers and reducing the range of dynamic hearing. This may protect against acoustic trauma.

Drugs associated with CHRNA10

Trimethaphan Camsylate

Target

CHRNA10

Mechanism

CHRNA10 antagonists

Active Org.-

Originator Org.

F. Hoffmann-La Roche Ltd.

Active Indication-

Inactive Indication

Hypertension

Drug Highest PhaseWithdrawn

First Approval Ctry. / Loc.

United States

First Approval Date26 Apr 1954

Clinical Trials associated with CHRNA10

NCT03028571

/ WithdrawnPhase 1IIT

Acute Sympathetic Blockade and Endogenous Glucose Production

The investigators will test the null hypothesis that there will be no changes in the insulin-mediated suppression of endogenous glucose production (EGP) in response to autonomic blockade. To test this hypothesis, the investigators propose to determine the role of the autonomic nervous system in hepatic insulin resistance.

Start Date17 Apr 2017

Sponsor / Collaborator

Vanderbilt University Medical Center

NCT00178919

/ CompletedNot ApplicableIIT

Cardiovascular Regulation: Autonomic/Metabolic Mechanisms PO1 HL56693, Project 4: Cardiovascular Regulation: Autonomic/Metabolic Mechanisms

The amount of blood flowing to the different parts of the body is regulated by the autonomic (automatic) nerves and by local factors produced by the blood vessels. Nitric oxide (NO) is one of the most important of these metabolic factors. If the production of NO is slowed or stopped the amount of blood to the different parts of the body is decreased. There is increasing knowledge that NO mechanisms are impaired in a number of medical conditions. NO function is reduced in patients with risk factors for atherosclerosis (hardening of the arteries) such as hypercholesterolemia (patients with high cholesterol), or diabetes mellitus, and is also impaired in smokers. This NO "deficiency" is believed to contribute to the greater cardiovascular risk that marks these patient populations. This study is designed to examine if endothelial nitric oxide is an important control mechanism of blood pressure under normal conditions, and if impairment of nitric oxide contributes to hypertension.

Start Date01 Aug 2002

Sponsor / Collaborator

Vanderbilt University

100 Clinical Results associated with CHRNA10

100 Translational Medicine associated with CHRNA10

0 Patents (Medical) associated with CHRNA10

104

Literatures (Medical) associated with CHRNA10

01 Jan 2025·Journal of Veterinary Internal Medicine

Salivary peptidomic profiling of chronic gingivostomatitis in cats by matrix‐assisted laser desorption/ionization‐time‐of‐flight mass spectrometry and nanoscale liquid chromatography‐tandem mass spectrometry

Article

Author: Jaresitthikunchai, Janthima ; Techangamsuwan, Somporn ; Roytrakul, Sittiruk ; Pornthummawat, Apisit ; Phaonakrop, Narumon ; Wardhani, Sabrina Wahyu ; Lacharoje, Sitthichok ; Ploypetch, Sekkarin

AbstractBackgroundChronic gingivostomatitis in cats (FCGS) is a moderately to severely painful condition, potentially caused by inadequate immune response to oral antigenic stimulation. Salivary peptidome analysis can identify inflammatory protein mediators and pathways involved in oral mucosal immune activation and may indicate potential therapeutic options for FCGS.ObjectiveEvaluate the diversity and abundance of salivary peptides in cats with FCGS using matrix‐assisted laser desorption/ionization‐time‐of‐flight mass spectrometry (MALDI‐TOF MS) and nanoscale liquid chromatography‐tandem mass spectrometry (nano LC‐MS/MS).AnimalsThirty‐two cats with FCGS and 18 healthy controls.MethodsCase‐control cross‐sectional study. We compared the salivary peptide profiles of diseased and healthy cats. The diagnosis of FCGS was confirmed by histopathology. Saliva samples were analyzed for viral infections using polymerase chain reaction (PCR), peptide mass fingerprint (PMF) using MALDI‐TOF MS, and peptide identification using nano LC‐MS/MS.ResultsDistinct clusters of peptide profiles were observed between groups. In FCGS, 26 salivary peptides were altered, including apolipoprotein A1, nuclear receptor subfamily 1 group I member 3, fibrinogen alpha chain, interleukin 2 receptor gamma, interleukin 23 receptor, hemoglobin subunit alpha, and serpin peptidase inhibitor clade A (alpha‐1 antiproteinase, antitrypsin) member 12, protein‐tyrosine‐phosphatase, and cholinergic receptor nicotinic alpha 10 subunit. Protein‐anti‐inflammatory drug interaction networks were observed.Conclusions and Clinical ImportancePeptide mass fingerprint and peptide profiles identified distinct clusters between FCGS and healthy cats. The 9 novel salivary peptide markers were associated with the JAK/STAT and PI3K/Akt pathways and immune responses. These potentially noninvasive biomarkers may facilitate understanding of FCGS pathophysiology and guide future therapeutic research.

01 Dec 2023·Molecular and Cellular Neuroscience

An in-depth association analysis of genetic variants within nicotine-related loci: Meeting in middle of GWAS and genetic fine-mapping

Article

Author: Zhang, Yuan ; Kochunov, Peter ; Hong, L Elliot ; Bi, Chuan ; Ye, Zhenyao ; Pan, Yezhi ; Liu, Song ; Wu, Qiong ; Ma, Tianzhou ; Chen, Shuo ; Mitchell, Braxton ; Mo, Chen

In the last two decades of Genome-wide association studies (GWAS), nicotine-dependence-related genetic loci (e.g., nicotinic acetylcholine receptor - nAChR subunit genes) are among the most replicable genetic findings. Although GWAS results have reported tens of thousands of SNPs within these loci, further analysis (e.g., fine-mapping) is required to identify the causal variants. However, it is computationally challenging for existing fine-mapping methods to reliably identify causal variants from thousands of candidate SNPs based on the posterior inclusion probability. To address this challenge, we propose a new method to select SNPs by jointly modeling the SNP-wise inference results and the underlying structured network patterns of the linkage disequilibrium (LD) matrix. We use adaptive dense subgraph extraction method to recognize the latent network patterns of the LD matrix and then apply group LASSO to select causal variant candidates. We applied this new method to the UK biobank data to identify the causal variant candidates for nicotine addiction. Eighty-one nicotine addiction-related SNPs (i.e.,-log(p) > 50) of nAChR were selected, which are highly correlated (average r²>0.8) although they are physically distant (e.g., >200 kilobase away) and from various genes. These findings revealed that distant SNPs from different genes can show higher LD r² than their neighboring SNPs, and jointly contribute to a complex trait like nicotine addiction.

01 Jun 2023·eneuro

Hyperconnectivity of Two Separate Long-Range Cholinergic Systems Contributes to the Reorganization of the Brain Functional Connectivity during Nicotine Withdrawal in Male Mice

Article

Author: Davoudian, Pasha A ; Kwan, Alex C ; George, Olivier ; Kimbrough, Adam ; Collazo, Andres ; Carrette, Lieselot L G

Chronic nicotine results in dependence with withdrawal symptoms on discontinuation of use, through desensitization of nicotinic acetylcholine receptors and altered cholinergic neurotransmission. Nicotine withdrawal is associated with increased whole-brain functional connectivity and decreased network modularity; however, the role of cholinergic neurons in those changes is unknown. To identify the contribution of nicotinic receptors and cholinergic regions to changes in the functional network, we analyzed the contribution of the main cholinergic regions to brain-wide activation of the immediate early-gene Fos during withdrawal in male mice and correlated these changes with the expression of nicotinic receptor mRNA throughout the brain. We show that the main functional connectivity modules included the main long-range cholinergic regions, which were highly synchronized with the rest of the brain. However, despite this hyperconnectivity, they were organized into two anticorrelated networks that were separated into basal forebrain-projecting and brainstem-thalamic-projecting cholinergic regions, validating a long-standing hypothesis of the organization of the brain cholinergic systems. Moreover, baseline (without nicotine) expression ofChrna2,Chrna3,Chrna10, andChrndmRNA of each brain region correlated with withdrawal-induced changes in Fos expression. Finally, by mining the Allen Brain mRNA expression database, we were able to identify 1755 gene candidates and three pathways (Sox2-Oct4-Nanog, JAK-STAT, and MeCP2-GABA) that may contribute to nicotine withdrawal-induced Fos expression. These results identify the dual contribution of the basal forebrain and brainstem-thalamic cholinergic systems to whole-brain functional connectivity during withdrawal; and identify nicotinic receptors and novel cellular pathways that may be critical for the transition to nicotine dependence.

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CHRNA10

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