Related Experiment Video
Updated: May 5, 2026
In vitro Measurements of Tracheal Constriction Using Mice
Published on: June 25, 2012
The mechanism of Ptychodiscus brevis toxin-induced rat vas deferens contraction
Abstract:
Ptychodiscus brevis, which causes Florida red tide, produces Ptychodiscus brevis toxin (PBTX) known to contain neurotoxins and to induce rhinorrhea, tearing, and cough in normal humans and wheezing in asthmatic subjects. It was previously reported (J Allergy Clin Immunol 69:418, 1982; 73:824, 1984) that PBTX causes canine tracheal smooth muscle contraction via stimulation of sodium channels in the axons of parasympathetic postganglionic nerves and the release of acetylcholine from these nerve endings. This was postulated to be an asthma-triggering mechanism. In this article the toxins were evaluated to determine if they also stimulate sodium channels on adrenergic nerve endings and release norepinephrine. Rat vas deferens was selected as the experimental tissue. Both PBTX and norepinephrine contracted rat vas deferens. Prazosin 10(-6) mol/L blocked the response to PBTX (3 micrograms/ml) (88.3% to 27.3% contraction [n = 6; p less than 0.001]) and the response to norepinephrine (EC50 was shifted from 1.67 X 10(-6) mol/L to 1.25 X 10(-4) mol/L in the presence of prazosin 10(-6) mol/L [n = 6; p less than 0.001]). Phentolamine 10(-6) mol/L also blocked both PBTX and norepinephrine. Tetrodotoxin 10(-7) mol/L, a sodium channel blocker, completely blocked the response to PBTX but not to norepinephrine. The response to PBTX was significantly reduced from 1.53 gm of tension in controls to 0.29 gm of tension (n = 6; p = 0.002) in tissues obtained from rats pretreated with reserpine (2 mg/kg per day for 2 days, injected intraperitoneally). Verapamil 10(-5) mol/L blocked the PBTX response, and PBTX caused no contraction in calcium-free media.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Florida red tide toxin (PBTX) stimulates adrenergic nerves, releasing norepinephrine and causing muscle contraction. This study investigates PBTX
Area of Science:
- Neuroscience
- Pharmacology
- Toxicology
Background:
- Ptychodiscus brevis toxin (PBTX) from Florida red tide causes neurotoxic effects.
- PBTX previously shown to stimulate parasympathetic nerves, releasing acetylcholine and causing smooth muscle contraction.
- This mechanism was proposed as a potential asthma trigger.
Purpose of the Study:
- To investigate if PBTX stimulates adrenergic nerve endings.
- To determine if PBTX causes the release of norepinephrine.
- To elucidate the mechanism of PBTX-induced muscle contraction in adrenergic pathways.
Main Methods:
- Experiments conducted on rat vas deferens tissue.
- Assessed PBTX and norepinephrine-induced contractions.
- Utilized alpha-adrenergic blockers (prazosin, phentolamine) and a sodium channel blocker (tetrodotoxin).
- Investigated the role of norepinephrine release using reserpine pretreatment.
- Examined calcium dependency of the PBTX response with verapamil and calcium-free media.
Main Results:
- PBTX and norepinephrine both induced contractions in rat vas deferens.
- Prazosin and phentolamine blocked PBTX-induced contractions, indicating adrenergic receptor involvement.
- Tetrodotoxin completely blocked PBTX response, confirming sodium channel stimulation.
- Reserpine pretreatment significantly reduced PBTX-induced tension, suggesting norepinephrine release.
- Verapamil blocked the PBTX response, and the response was absent in calcium-free media, indicating calcium influx is necessary.
Conclusions:
- PBTX stimulates sodium channels on adrenergic nerve endings.
- PBTX induces norepinephrine release from these nerve endings.
- The PBTX mechanism involves calcium influx and alpha-adrenergic receptor activation.
- Findings suggest a novel pathway for PBTX toxicity potentially contributing to respiratory symptoms.
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