Atropine methyl nitrate increases myenteric but not dorsal vagal complex Fos-like immunoreactivity in the rat

Shannon J Raboin1, Stephen Gulley, Sheryce C Henley

  • 1Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088, USA.

Physiology & Behavior
|June 27, 2006
PubMed

Insights

Atropine methyl nitrate increased Fos-like immunoreactivity in the rat myenteric plexus but not the dorsal vagal complex. This suggests the myenteric plexus locally mediates behavioral responses to atropine methyl nitrate.

Area of Science:

  • Neuroscience
  • Gastroenterology

Background:

  • Atropine methyl nitrate (AMN) is a drug with known effects on the gastrointestinal system.
  • Understanding the neural pathways involved in AMN's action is crucial for its therapeutic application.

Purpose of the Study:

  • To investigate the effects of AMN on neural activation, specifically Fos-like immunoreactivity (Fos-LI), in the rat enteric and central nervous systems.
  • To explore the potential role of the myenteric plexus versus the dorsal vagal complex in mediating AMN's behavioral effects.

Main Methods:

  • Adult male Sprague-Dawley rats were administered varying doses of AMN intraperitoneally.
  • Fos-like immunoreactivity (Fos-LI) was assessed in the myenteric plexus and the dorsal vagal complex (DVC), including the area postrema (AP), nucleus of the solitary tract (NTS), and dorsal motor nucleus of the vagus (DMV).
  • Sucrose intake was measured following AMN administration.

Main Results:

  • AMN administration (0.05, 0.5, and 25 mg/kg) significantly increased Fos-LI in the myenteric plexus.
  • No significant increase in Fos-LI was observed in the DVC (AP, NTS, DMV) across the tested AMN doses.
  • A 3 mg/kg dose of AMN reduced sucrose intake but did not alter Fos-LI in either the myenteric plexus or DVC.

Conclusions:

  • The myenteric plexus shows increased neural activation in response to AMN.
  • The dorsal vagal complex does not appear to be a primary site for AMN-induced neural signaling at the tested doses.
  • The myenteric plexus may play a localized role in mediating the behavioral effects of atropine methyl nitrate.

Related Concept Videos

Cholinergic Antagonists: Chemistry and Structure-Activity Relationship01:29

Cholinergic Antagonists: Chemistry and Structure-Activity Relationship

Cholinergic antagonists bind to cholinergic receptors and limit the effects of acetylcholine and other cholinergic agonists. Based on the specific cholinergic receptor affinity, these antagonists are classified as muscarinic or nicotinic. Anticholinergics interrupt parasympathetic innervations while sympathetic innervations remain uninterrupted. Muscarinic antagonists are also called 'muscarinic antagonists', 'antimuscarinics', or 'parasympatholytics'. Nicotinic antagonists are called...
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...
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...
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
Although all competitive neuromuscular blockers are designed...
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...
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...