neuromuscular junction

Amifampridine (3,4-Diaminopyridine) is primarily used to treat rare muscle diseases. It blocks potassium channel efflux in nerve terminals, increasing action potential duration, which allows Ca2+ channels to remain open longer and enhances acetylcholine release to stimulate muscles at the end plate.

Argireline (Acetyl hexapeptide-3) is a peptide composed of amino acid chains that significantly inhibits Ca2+-dependent neurotransmitter (acetylcholine) release at the neuromuscular junction, exhibiting notable anti-wrinkle and anti-aging activity[1][2][3].

1. Tuberostemonine (Tuberstemonine) exhibits relatively higher intestinal permeabilities. 2. Tuberostemonine acts in part as an open-channel blocker at the crayfish neuromuscular junction.

3- Deoxyaconitine is a derivative of Aconitine (A189875), which activates tetrodotoxin-sensitive Na+ channels, inducing presynaptic depolarization, thus blocking the nerve action potential which, in turn, blocks the release of neurotransmitters and decreases the end plate potential at the neuromuscular junction.

α-CGRP, rat TFA, a neuropeptide (calcitonin gene-related peptide (CGRP)) mainly expressed in neuromuscular junction, is a potent vasodilator. α-CGRP, rat TFA can lead to a fall in blood pressure and an increase in heart rate by peripheral administration, also relax colonie smooth muscle. α-CGRP, rat TFA has the potential in cardiovascular, pro-inflammatory, migraine and metabolic studies [1] [2] [3] .

Ambenonium chloride tetrahydrate is a salt of ambenonium --- a quaternary ammonium compound with parasympathomimetic activity. It is a cholinesterase inhibitor used in the management of myasthenia gravis. Myasthenia gravis occurs when the body produces antibodies against acetylcholine receptors, and thus inhibits signal transmission across the myoneural junction. Ambenonium chloride is a rapid indirect-acting cholinergic agonist that reversibly blocks the activity of acetylcholinesterase, thereby prevents acetylcholine hydrolysis and prolonging its activity on nicotinic receptors at the neuromuscular junction.

Botulinum toxin type B, an antigen-specific exotoxin produced by the anaerobic bacterium Clostridium botulinum, is utilized in the study of neck dystonia. It inhibits the release of Acetylcholine from the neuromuscular junction, causing relaxation paralysis or muscle weakening in the targeted muscle [1].

Ambenonium Chloride is the chloride salt form of ambenonium, a quaternary ammonium compound with parasympathomimetic activity. It is a cholinesterase inhibitor used in the management of myasthenia gravis. Myasthenia gravis occurs when the body produces antibodies against acetylcholine receptors, and thus inhibits signal transmission across the myoneural junction. Ambenonium chloride is a rapid indirect-acting cholinergic agonist that reversibly blocks the activity of acetylcholinesterase, thereby prevents acetylcholine hydrolysis and prolonging its activity on nicotinic receptors at the neuromuscular junction.

Leucomyosuppressin, isolated from head extracts of the cockroach Leucophaea maderae, inhibits evoked transmitter release at the mealworm neuromuscular junction.

Brevetoxin B is a polyketide neurotoxin produced by Karenia species and other dinoflagellates. It binds to site 5 on the alpha subunit of voltage-gated sodium channels (IC50 = 15 nM) on neurons at the neuromuscular junction, causing the channel to open irreversibly at potentials more negative than normal, discharging action potentials repetitively. Brevetoxin B is ichthyotoxic at nanomolar concentrations and is responsible for an illness described as neurotoxic shellfish poisoning.