How does a Bungarotoxin work?

How does a Bungarotoxin work?

Toxin mechanism Bungarotoxins function by modulating acetylcholine neurotransmission in both muscles and neurons. α-Bungarotoxin irreversibly blocks the binding of acetylcholine (ACh) to postsynaptic nicotinic acetylcholine receptors (nAchR) on both muscle and neurons.

Is Bungarotoxin an agonist or antagonist?

The snake neurotoxin α-bungarotoxin (α-Bgtx) is a competitive antagonist at nicotinic acetylcholine receptors (nAChRs) and is widely used to study their function and cell-surface expression.

How does krait snake venom work?

The venom of kraits contains three major types of neurotoxin. α-Bungarotoxins cause a failure of neuromuscular transmission by binding to post-synaptic nAChR at the neuromuscular junction (NMJ).

How does Alpha Conotoxin work?

α-conotoxin inhibits nicotinic acetylcholine receptors at nerves and muscles. δ-conotoxin inhibits fast inactivation of voltage-dependent sodium channels.

Is Bungarotoxin a protein?

It is a type of α-neurotoxin, a neurotoxic protein that is known to bind competitively and in a relatively irreversible manner to the nicotinic acetylcholine receptor found at the neuromuscular junction, causing paralysis, respiratory failure, and death in the victim.

What do nicotinic acetylcholine receptors do?

The nicotinic acetylcholine receptor is a transmembrane allosteric protein that mediates transduction of chemoelectric signals throughout the nervous system by opening an intrinsic ionic channel. This rapid pore opening enables flow of Na+, K+, and, in several instances, Ca2+ ions across the cell membrane.

Is krait neurotoxic?

Common krait (Bungarus caeruleus) is distributed throughout South Asia, and is responsible for large numbers of cases of severe neurotoxic envenoming each year[4]. It results in a descending flaccid paralysis progressing to life threatening respiratory paralysis unless mechanical ventilation is available[5–7].

How do the following toxins Bungarotoxin and Conotoxin cause paralysis?

Venomous and Poisonous Animals Post-synaptic (curaremimetic) neurotoxins, or α-neurotoxins, such as α-bungarotoxin and cobrotoxin bind to nicotinic acetylcholine receptors at the motor end-plates of skeletal muscles, causing generalized flaccid paralysis and death from bulbar and respiratory muscle weakness.

How does conotoxin affect the nervous system?

Conotoxins, found in sea cone snails, are used by these organisms for predatory purposes: they paralyze their prey by blocking or inhibiting various targets of the nervous system.

Where would α conotoxin have its effect?

One family of conopeptides, the α-conotoxins, specifically target different isoforms of nicotinic acetylcholine receptors (nAChRs) found both in the neuromuscular junction and central nervous system.

What is the mechanism of action of β-bungarotoxin on the frog?

At the frog neuromuscular junction, β-bungarotoxin produces a triphasic effect on evoked and spontaneous release of acetylcholine. An initial inhibition is followed by a substantial increase in the frequency of mepps and in the evoked epp.

How does β-bungarotoxin affect the neuromuscular junction?

At the frog neuromuscular junction, β-bungarotoxin produces a triphasic effect on evoked and spontaneous release of acetylcholine. An initial inhibition is followed by a substantial increase in the frequency of mepps and in the evoked epp. The mepps are unchanged in amplitude and shape.

What is the difference between β-bungarotoxin and crotoxin?

Of these, β-bungarotoxin (e.g., venom of kraits) acts on the voltage-dependent potassium channel, while crotoxin (venom of South American rattlesnakes, e.g., Crotalus durissus terrificus) binds to a not yet identified protein membrane (Chippaux, 2006; Doley et al., 2010).