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Cholinergic Receptors: Muscarinic01:25

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The pharmacological actions of acetylcholine are elicited via its binding to two families of cholinergic receptors or cholinoceptors, namely, muscarinic and nicotinic receptors. Muscarinic receptors are G protein-coupled receptors and have five subtypes, M1–M5. All mAChR subtypes are activated by acetylcholine and blocked by the antagonist, atropine. 
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Asthma: Pathogenesis and Management01:20

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Asthma is a chronic pulmonary condition involving inflammation of the airways, hyper-reactivity, and reversible obstruction of the airways. This condition can significantly impact a person's quality of life, making breathing difficult and leading to distressing symptoms.
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Asthma-II: Pathophysiology and Classification01:26

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Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
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Parasympathetic Signaling01:30

Parasympathetic Signaling

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Parasympathetic signaling plays a crucial role in regulating various physiological processes. It involves the release of acetylcholine (ACh) by parasympathetic neurons, which can have localized and short-lived effects. The majority of ACh released is rapidly inactivated at the synapse by the enzyme acetylcholinesterase (AChE), which hydrolyzes Ach into choline and acetate. Additionally, the tissue cholinesterase deactivates any ACh diffusing into the surrounding tissues.
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Cholinergic agonists or cholinomimetics mimic the action of acetylcholine to stimulate the parasympathetic nervous system. They are categorized into direct-acting and indirect-acting agents. The direct-acting cholinergic drugs induce the parasympathetic response by directly binding to the muscarinic or nicotine receptors. In comparison, the indirect-acting cholinergic drugs prevent acetylcholine hydrolysis, indirectly contributing to the extended parasympathetic response.
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Direct-Acting Cholinergic Agonists: Pharmacological Actions00:59

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Direct-acting cholinergic agonists exert their pharmacological actions by mimicking the effects of acetylcholine on postsynaptic muscarinic receptors to generate parasympathetic responses. These agents elicit a range of physiological responses, including cardiovascular effects. For example, activation of muscarinic receptors induces bradycardia, decreased cardiac output, reduced peripheral resistance, and consequent hypotension. In the eye, stimulation of M3 receptors leads to smooth muscle...
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Cholinergic Synapse Pathway Gene Polymorphisms Associated With Late-Phase Responses in Allergic Rhinitis.

Simranjit K Samra1,2,3, Ashwini Rajasekaran2,3, Andrew J Sandford1,2,4

  • 1Experimental Medicine, University of British Columbia, Vancouver, BC, Canada.

Frontiers in Allergy
|April 7, 2022
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Summary

This study links genetic variations in cholinergic synapse pathway genes to persistent nasal congestion in allergic rhinitis (AR). These findings may help in understanding the late-phase response (LPR) in AR.

Keywords:
allergic rhinitisenvironmental exposure unitgeneticsinflammationlate-phase responsenasal congestion

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Area of Science:

  • Immunology
  • Genetics
  • Pharmacology

Background:

  • Allergic rhinitis (AR) involves early-phase (EPR) and late-phase responses (LPR).
  • Cholinergic synapse pathway genes are implicated in late asthmatic responses.
  • Nasal congestion is a key symptom of the LPR in AR.

Purpose of the Study:

  • Investigate polymorphisms in cholinergic synapse pathway genes in relation to the LPR of AR.
  • Sub-phenotype AR participants based on nasal congestion severity and duration.
  • Explore the association between genetic variations and gene expression in AR subtypes.

Main Methods:

  • Allergen exposure in a controlled Environmental Exposure Unit for 20 healthy and 74 AR participants.
  • Sub-phenotyping AR participants into acute congestion (AC) and persistent congestion (PC) groups.
  • Genotyping and gene expression assays on blood samples to analyze SNPs in cholinergic pathway genes.

Main Results:

  • Significant differences in allele frequencies of 25 SNPs across seven genes (ADCY3, AKT3, CACNA1S, CHRM3, CHRNB2, GNG4, KCNQ4) between PC and AC groups (P < 0.10).
  • PC participants exhibited increased minor allele content in these 25 SNPs (P = 0.009).
  • Two SNPs in AKT3 were associated with altered gene expression in PC participants (FDR < 0.01).

Conclusions:

  • Identified an association between LPR in AR and polymorphisms in cholinergic synapse pathway genes.
  • Developed a novel method for sub-phenotyping AR using self-reported nasal congestion scores.
  • Suggests a genetic basis for persistent symptoms in AR, potentially influencing LPR development.