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Related Concept Videos

Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:22

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...
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 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: Therapeutic Uses01:11

Direct-Acting Cholinergic Agonists: Therapeutic Uses

Direct-acting cholinergic agonists have many therapeutic uses in various medical fields. Choline esters, including acetylcholine, have limited clinical utility due to their non-selectivity and short duration of action. Still, acetylcholine and carbachol are applied topically during ophthalmologic surgery to induce miosis. Pilocarpine, a muscarinic and ganglionic stimulator, effectively treats open-angle glaucoma and alleviates xerostomia and dry mouth caused by radiotherapy or Sjögren syndrome.
Direct-Acting Cholinergic Agonists: Pharmacokinetics01:31

Direct-Acting Cholinergic Agonists: Pharmacokinetics

Direct-acting cholinergic agonists, such as synthetic choline esters and naturally occurring alkaloids, exert their effects by enhancing the actions of acetylcholine and stimulating the parasympathetic nervous system. Synthetic choline esters share structural similarities with acetylcholine. For example, they have a positively charged quaternary ammonium or onium group, contributing to their hydrophilic characteristics. As a result, they are poorly absorbed in the body through oral...
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants


Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...

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Updated: Jun 27, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
10:39

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

Published on: June 2, 2014

Morphine increases acetylcholine release in the trigeminal nuclear complex.

Zhenghong Zhu1, Heather R Bowman, Helen A Baghdoyan

  • 1Department ofAnesthesiology, University of Michigan, Ann Arbor, MI 48109-5615, USA.

Sleep
|December 19, 2008
PubMed
Summary
This summary is machine-generated.

Opioids like morphine increase acetylcholine release in the trigeminal nuclei (PSTN and MoV) through kappa opioid receptors, suggesting synaptic disinhibition may explain pain relief.

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Intracranial Pharmacotherapy and Pain Assays in Rodents
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Published on: June 2, 2014

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Intracranial Pharmacotherapy and Pain Assays in Rodents
02:26

Intracranial Pharmacotherapy and Pain Assays in Rodents

Published on: April 9, 2019

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • The trigeminal nuclear complex (V) is crucial for facial sensation and mastication.
  • Opioid analgesics are used for trigeminal pathologies, but their effect on acetylcholine (ACh) release in V is unknown.

Purpose of the Study:

  • To investigate the effect of opioids on ACh release in the principal sensory trigeminal nucleus (PSTN) and trigeminal motor nucleus (MoV).
  • To test the hypothesis that microdialysis delivery of opioids alters ACh release in PSTN and MoV.

Main Methods:

  • Wistar rats (n=53) underwent microdialysis in PSTN and MoV.
  • ACh release was measured following administration of various agents, including morphine, DAMGO, naloxone, nor-BNI, tetrodotoxin, bethanechol, and bicuculline.

Main Results:

  • Morphine and bethanechol increased ACh release in PSTN in a concentration-dependent manner.
  • Morphine increased ACh release in MoV.
  • The morphine effect in PSTN was blocked by nor-BNI (kappa opioid antagonist) but not naloxone (mu opioid antagonist).
  • Tetrodotoxin reduced ACh release, confirming its release is action potential-dependent.
  • Bicuculline increased ACh release in PSTN.

Conclusions:

  • This study provides the first direct measurements of ACh release in PSTN and MoV.
  • Opioid-induced increases in ACh release in the trigeminal nuclei may involve synaptic disinhibition, potentially mediated by kappa opioid receptors.