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Cholinergic Receptors: Muscarinic

Cholinergic Receptors: Muscarinic

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.
The subtypes M1, M3, and M5 couple with the Gq subunit and activate the phospholipase C (PLC) activity, mobilizing intracellular Ca2+. Activation...

Direct-Acting Cholinergic Agonists: Pharmacological Actions

Direct-Acting Cholinergic Agonists: Pharmacological Actions

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...

Parasympathetic Signaling

Parasympathetic Signaling

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.
The effects of...

Cholinergic Receptors: Nicotinic

Cholinergic Receptors: Nicotinic

Nicotinic receptors are ligand-gated ion channels that are activated by acetylcholine and nicotine. Upon activation, they cause a rapid increase in the permeability of cells to K+, Na+, and Ca2+, followed by depolarization and excitation. They are in the autonomic ganglia, skeletal neuromuscular junction, CNS, and adrenal medulla.
There are two types of nicotinic receptors: neuromuscular (NM/NM/N1) and neuronal (NN/NN/N2). The two families differ based on their location and selectivity to...

Cholinergic Antagonists: Pharmacological Actions

Cholinergic Antagonists: Pharmacological Actions

Antimuscarinic drugs block muscarinic receptors in multiple systems, including the gut, eye, smooth muscles, respiratory tract, cardiovascular, and central nervous systems. They produce similar effects with varying selectivity depending on the specific agent and tissue. Here are the key pharmacological actions of antimuscarinics:
Gastrointestinal Effects: Antimuscarinics reduce gut contractions, increase gastric emptying, and slow intestinal transit. They partly inhibit gastric acid secretion...

Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship

Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship

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.
The direct-acting...

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Related Experiment Video

Updated: Jun 23, 2026

In vitro Measurements of Tracheal Constriction Using Mice

In vitro Measurements of Tracheal Constriction Using Mice

Published on: June 25, 2012

Mast cell-cholinergic nerve interaction in mouse airways.

Letitia A Weigand¹, Allen C Myers, Sonya Meeker

¹Department of Medicine, Johns Hopkins University, Baltimore, MD, USA.

The Journal of Physiology

|May 1, 2009

Summary

Antigen-induced mouse trachea contraction requires mast cell-derived serotonin (5-HT) to activate 5-HT(2) receptors on parasympathetic neurons, leading to airway smooth muscle contraction. This process is epithelium-independent.

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Published on: July 10, 2018

Area of Science:

Immunology
Neuroscience
Pharmacology

Background:

Antigen challenge in sensitized individuals can trigger airway smooth muscle contraction.
The precise cellular and molecular mechanisms underlying antigen-induced airway contraction are not fully elucidated.
Mast cells and their mediators are implicated in allergic airway responses.

Purpose of the Study:

To investigate the mechanism of antigen-induced trachea contraction in actively sensitized mice.
To determine the role of mast cells and serotonin in this contractile response.
To identify the specific receptors and neuronal pathways involved.

Main Methods:

Isolation of mouse trachea from ovalbumin-sensitized C57BL/6J and mast cell-deficient (sash -/-) mice.
Measurement of smooth muscle contraction and histamine release upon ovalbumin (OVA) challenge.
Pharmacological assessment using 5-HT, ketanserin (5-HT(2) receptor antagonist), and atropine.
Epithelial denudation experiments.
Histological analysis of mast cell distribution.
Intracellular recordings of parasympathetic neuron membrane potential in tracheal ganglia.

Main Results:

Ovalbumin induced rapid, short-lived smooth muscle contraction and histamine release in sensitized mouse trachea.
Contraction was mimicked by 5-HT and inhibited by ketanserin and atropine.
Epithelial denudation did not affect OVA-induced contraction.
OVA failed to induce contraction or histamine release in mast cell-deficient mice.
OVA and 5-HT caused ketanserin-sensitive depolarization of parasympathetic neurons.

Conclusions:

Antigen-induced contraction of mouse trachea is epithelium-independent.
Mast cell-derived serotonin (5-HT) is essential for this response.
5-HT activates 5-HT(2) receptors on parasympathetic cholinergic neurons.
This activation leads to acetylcholine release and subsequent airway smooth muscle contraction.