Related Experiment Video

Updated: Aug 15, 2026

The Use of Cystometry in Small Rodents: A Study of Bladder Chemosensation
08:08

The Use of Cystometry in Small Rodents: A Study of Bladder Chemosensation

Published on: August 21, 2012

Muscarinic cholinergic receptors in area postrema and brainstem areas regulating emesis

N W Pedigo, K R Brizzee

    Brain Research Bulletin
    |February 1, 1985
    PubMed

    Insights

    Central cholinergic pathways in the brainstem regulate motion sickness. This study found muscarinic receptors in key areas like the vagal nuclear complex and area postrema, suggesting potential antiemetic drug targets.

    Area of Science:

    • Neuroscience
    • Pharmacology
    • Gastroenterology

    Background:

    • Central cholinergic pathways are crucial for processing motion stimuli and triggering motion sickness symptoms like nausea and vomiting.
    • Specific brainstem regions, including the area postrema (AP), vagal nuclear complex (VNC), reticular formation (RF), and vestibular complex (VC), are implicated in mediating motion-induced emesis.

    Purpose of the Study:

    • To biochemically and pharmacologically characterize muscarinic cholinergic receptors in the bovine brainstem using 3H-QNB binding.
    • To investigate the distribution and properties of these receptors in brainstem regions involved in emesis.

    Main Methods:

    • Histological examination of bovine and squirrel monkey brainstem structures.
    • Radioligand binding assays using 3H-QNB to quantify muscarinic receptor density and affinity (Scatchard analysis, saturation, and kinetic experiments).
    • Pharmacological profiling of cholinergic agonists and antagonists.
    • Testing the antiemetic activity of drugs in a squirrel monkey model of motion-induced emesis.

    Main Results:

    • Muscarinic receptors showed an uneven distribution in the bovine brainstem, with high densities in the VNC and AP, intermediate levels in the RF, and low concentrations in the VC.
    • Dissociation constants for 3H-QNB were consistent across all studied brainstem regions.
    • The pharmacological profiles of cholinergic agents were similar to those reported for muscarinic receptors elsewhere.
    • Several drugs that inhibited 3H-QNB binding demonstrated antiemetic effects in the squirrel monkey model.

    Conclusions:

    • Muscarinic receptors are unevenly distributed in the bovine brainstem regions regulating emesis.
    • The antiemetic properties of certain drugs may stem from their antagonism of brainstem muscarinic receptors involved in emesis pathways.
    • This research provides a foundation for developing targeted anti-motion sickness therapies by modulating central cholinergic signaling.

    More Related Videos

    Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology10:26

    Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology

    Published on: August 18, 2014

    A Method of Nodose Ganglia Injection in Sprague-Dawley Rat09:28

    A Method of Nodose Ganglia Injection in Sprague-Dawley Rat

    Published on: November 25, 2014

    Related Concept Videos

    Cholinergic Receptors: Muscarinic01:25

    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 Actions00:59

    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...
    Cholinergic Antagonists: Pharmacological Actions01:28

    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...
    Cholinergic Antagonists: Therapeutic Uses01:26

    Cholinergic Antagonists: Therapeutic Uses

    Antimuscarinic drugs have various therapeutic applications by inhibiting parasympathetic stimulation in different systems. Here are the key therapeutic uses of antimuscarinics:    
    Respiratory Tract: Ipratropium, aclidinium, and tiotropium treat asthma, chronic bronchitis, and chronic obstructive pulmonary disease (COPD). They protect against bronchoconstriction caused by irritants like cigarette smoke, sulfur dioxide, and ozone. They also help reduce nasopharyngeal secretions in common...
    Parasympathetic Signaling01:30

    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...
    Pathophysiology of Vomiting01:22

    Pathophysiology of Vomiting

    Vomiting is a complex physiological response to expel harmful or irritating substances from the body. It's a defensive mechanism triggered by stimuli like poisons, microbial toxins, cytotoxic drugs, and mechanical abdominal distension. The process is centrally coordinated by the vomiting (or emetic) center located in the medulla of the brainstem. This area, rich in muscarinic M1, histamine H1, neurokinin 1 (NK1), and serotonin 5-HT3 receptors, coordinates the act of vomiting through interaction...