Mohamed Naguib, in Complications in Anesthesia Second EditionDefinition Neuromuscular transmission is dependent on a coordinated mechanism involving 1 synthesis, storage, and release of acetylcholine from the presynaptic motor nerve endings at the neuromuscular junction; 2 binding of acetylcholine to nicotinic receptors on the postsynaptic region of the muscle membrane, with consequent generation of the action potential; and 3 rapid hydrolysis of acetylcholine by acetylcholinesterase enzyme present in the synaptic cleft. Autoimmune or genetic defects at the presynaptic region, synaptic basal lamina, or postsynaptic structure of the neuromuscular junction can compromise the safety margin of neuromuscular transmission. This can result in a diverse array of myasthenic disorders Fig.
Some toxins, such as the botulin toxin, act on the presynaptic side of the junction. They prevent it from releasing acetylcholine and thus produce an effect of muscle weakness or paralysis.
Other toxins, however, act directly on the nicotinic receptor. They occupy the acetylcholine-binding site but do not cause the channel to open.
Hence the acetylcholine that has been released into the synaptic gap cannot bind to the receptors, so the muscle cannot contract. This is how curare works the poison in which Amazon Indians dip their arrows: This same mechanism is at work with bungarotoxin, a type of snake venom.
Still other toxic substances lodge in the central channel of the The neuromuscular junction receptor, thus blocking the passage of ions. This is what happens with procaine, lidocaine, and benzocaine, all of which are molecules used in local anesthesia, as well as with tetrodotoxin, a toxin that is found in the livers of certain fish and that can cause death within a few hours of ingestion.
Each of these receptors consists of 5 subunits that form a pentagonal structure around a central channel. Ions and Ion Channels The nicotinic receptor is a channel or ionotropic receptor: When one of these substances binds to the receptor, the channel opens, allowing many sodium ions to enter the post-synaptic cell and a few potassium ions to leave it, thus depolarizing it.
There are two types of nicotinic receptors: N1, found in the autonomic nervous system, and N2, found at neuromuscular junctions.
In addition to nicotinic receptors, there is another family of acetylcholine receptors, the muscarinic receptors. They belong to another large class of receptors called G-protein or metabotropic receptors.
The receptors in this class which includes dopamine receptors, for exampleare totally separate from the ion channels. They exert their effects on these channels via a protein located on the cytoplasmic side of the cell, known as G-protein because it binds GTP.
When a neurotransmitter binds to and activates a G-protein receptor, this receptor in turn activates this G-protein, which controls the opening of the physically separate ion channels, either directly or indirectly via a second messenger.
G-protein receptors therefore act more slowly than nicotinic receptors, where everything is centralized on the same protein complex. Also, whereas nicotinic receptors are composed of five distinct peptides, the seven transmembrane domains of muscarinic receptors all come from a single protein that snakes its way back and forth across the membrane.
There are at least five different types of muscarinic receptors, all of which can be activated by muscarine, a molecule produced by a mushroom. M1 and M3 receptors, for example, activate phospholipase C, a second messenger that brings about depolarization by opening calcium channels while reducing the flow of potassium.
In the brain, M1 receptors are found in the cortex and the central grey nuclei, while M3 receptors are found in the cerebellum. Both types of receptors are also involved in exocrine gland secretions. The action mechanism for type M2 receptors is different.
These receptors are coupled with a G-protein that inhibits adenyl cyclase. The reduction in the activity of this enzyme reduces the amount of the second messenger cyclical AMP, allowing the potassium channels to open and hyperpolarizing the cell. M2 receptors are also found not only in the central nervous system cerebellum, central grey nuclei, and brainstem but also in the heart.Oct 29, · A neuromuscular junction is a place in the body where the axons of motor nerves meet the muscle, allowing them to transmit messages from the brain that cause the muscle to contract and relax.
Every organism has thousands of these junctions that control the movements of the body and cause the heart to beat. A neuromuscular junction (or myoneural junction) is a chemical synapse formed by the contact between a motor neuron and a muscle fiber.
It is at the neuromuscular junction that a motor neuron is able to transmit a signal to . Neuromuscular junction disease is a medical condition where the normal conduction through the neuromuscular junction fails to function correctly.
The synapse or connection between a motor neuron and a skeletal muscle is known as neuromuscular junction. Communication happens between the neuron and muscle via nerve cells. Due to this communication or transmission of signal, the muscle is able to contract or relax.
Learn neuromuscular junction with free interactive flashcards. Choose from different sets of neuromuscular junction flashcards on Quizlet. myoneural junction (neuromuscular junction) the site of junction of a motor nerve fiber and a skeletal muscle fiber that it innervates.
The discoid expansion of the terminal branch of the axon forms the motor end plate, the neurotransmitter that diffuses across the synapse is acetylcholine.