Neuromuscular junction in the context of "Acetylcholinesterase"

A motor neuron (or motoneuron), also known as efferent neuron is a neuron that allows for both voluntary and involuntary movements of the body through muscles and glands. Its cell body is located in the motor cortex, brainstem or the spinal cord, and whose axon (fiber) projects to the spinal cord or outside of the spinal cord to directly or indirectly control effector organs, mainly muscles and glands. There are two types of motor neuron – upper motor neurons and lower motor neurons. Axons from upper motor neurons synapse onto interneurons in the spinal cord and occasionally directly onto lower motor neurons. The axons from the lower motor neurons are efferent nerve fibers that carry signals from the spinal cord to the effectors. Types of lower motor neurons are alpha motor neurons, beta motor neurons, and gamma motor neurons.

A single motor neuron may innervate many muscle fibres and a muscle fibre can undergo many action potentials in the time taken for a single muscle twitch. Innervation takes place at a neuromuscular junction and twitches can become superimposed as a result of summation or a tetanic contraction. Individual twitches can become indistinguishable, and tension rises smoothly eventually reaching a plateau.

Chemical synapses are biological junctions through which neurons' signals can be sent to each other and to non-neuronal cells such as those in muscles or glands. Chemical synapses allow neurons to form circuits within the central nervous system. They are crucial to the biological computations that underlie perception and thought. They allow the nervous system to connect to and control other systems of the body.

At a chemical synapse, one neuron releases neurotransmitter molecules into a small space (the synaptic cleft) that is adjacent to the postsynaptic cell (e.g., another neuron). The neurotransmitter molecules are contained within small sacs called synaptic vesicles, and are released into the synaptic cleft by exocytosis. These molecules then bind to neurotransmitter receptors on the postsynaptic cell. Finally, to terminate its action, the neurotransmitter is cleared from the cleft through one of several mechanisms, including enzymatic degradation or re-uptake, by specific transporters, either into the presynaptic cell or to neuroglia.

Botulinum toxin, botulinum neurotoxin, or botox is a neurotoxic protein produced by the bacterium Clostridium botulinum and related species, and it is the deadliest known substance ever recorded in the chemical literature. It prevents the release of the neurotransmitter acetylcholine from axon endings at the neuromuscular junction, thus causing flaccid paralysis. The toxin causes the disease botulism. The toxin is also used commercially for medical and cosmetic purposes. Botulinum toxin is an acetylcholine release inhibitor and a neuromuscular blocking agent.

The seven main types of botulinum toxin are named types A to G (A, B, C1, C2, D, E, F and G). New types are occasionally found. Types A and B are capable of causing disease in humans, and are also used commercially and medically. Types C–G are less common; types E and F can cause disease in humans, while the other types cause disease in other animals.

Orthotics (Greek: Ορθός, romanized: ortho, lit. 'to straighten, to align') also known as orthology is a medical specialty that focuses on the design and application of orthoses, sometimes known as braces, calipers, or splints. An orthosis is "an externally applied device used to influence the structural and functional characteristics of the neuromuscular and skeletal systems." Orthotists are medical professionals who specialize in designing orthotic devices such as braces or foot orthoses.

Weakness is a symptom of many different medical conditions. The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis.

Muscle weakness is a lack of muscle strength. Its causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis. Muscle weakness can also be caused by low levels of potassium and other electrolytes within muscle cells. It can be temporary or long-lasting (from seconds or minutes to months or years). The term myasthenia is from my- from Greek μυο meaning "muscle" + -asthenia ἀσθένεια meaning "weakness".

Nicotinic acetylcholine receptors, or nAChRs, are receptor polypeptides that respond to the neurotransmitter acetylcholine. Nicotinic receptors also respond to drugs such as the agonist nicotine. They are found in the central and peripheral nervous system, muscle, and many other tissues of many organisms. At the neuromuscular junction they are the primary receptor in muscle for motor nerve-muscle communication that controls muscle contraction. In the peripheral nervous system: (1) they transmit outgoing signals from the presynaptic to the postsynaptic cells within the sympathetic and parasympathetic nervous system; and (2) they are the receptors found on skeletal muscle that receives acetylcholine released to signal for muscular contraction. In the immune system, nAChRs regulate inflammatory processes and signal through distinct intracellular pathways. In insects, the cholinergic system is limited to the central nervous system.

The nicotinic receptors are considered cholinergic receptors, because they respond to acetylcholine. Nicotinic receptors get their name from nicotine, which selectively binds to nicotinic receptors but not to other acetylcholine receptors. (The other type of acetylcholine receptor, the muscarinic receptor, likewise gets its name from a chemical that selectively attaches to that receptor: muscarine. Acetylcholine itself binds to both muscarinic and nicotinic acetylcholine receptors.)

Diplopia is the simultaneous perception of two images of a single object that may be displaced in relation to each other. Also called double vision, it is a loss of visual focus under regular conditions, and is often voluntary. However, when occurring involuntarily, it results from impaired function of the extraocular muscles, where both eyes are still functional, but they cannot turn to target the desired object. Problems with these muscles may be due to mechanical problems, disorders of the neuromuscular junction, disorders of the cranial nerves (III, IV, and VI) that innervate the muscles, and occasionally disorders involving the supranuclear oculomotor pathways or ingestion of toxins.

Diplopia can be one of the first signs of a systemic disease, particularly to a muscular or neurological process, and it may disrupt a person's balance, movement, or reading abilities.

Acetylcholine (ACh) is an organic compound that functions in the brain and body of many types of animals (including humans) as a neurotransmitter. Its name is derived from its chemical structure: it is an ester of acetic acid and choline. Parts in the body that use or are affected by acetylcholine are referred to as cholinergic.

Acetylcholine is the neurotransmitter used at the neuromuscular junction. In other words, it is the chemical that motor neurons of the nervous system release in order to activate muscles. This property means that drugs that affect cholinergic systems can have very dangerous effects ranging from paralysis to convulsions. Acetylcholine is also a neurotransmitter in the autonomic nervous system, both as an internal transmitter for both the sympathetic and the parasympathetic nervous system, and as the final product released by the parasympathetic nervous system. Acetylcholine is the primary neurotransmitter of the parasympathetic nervous system.

Axon terminals (also called terminal boutons, synaptic boutons, end-feet, or presynaptic terminals) are distal terminations of the branches of an axon. An axon, also called a nerve fiber, is a long, slender projection of a nerve cell that conducts electrical impulses called action potentials away from the neuron's cell body to transmit those impulses to other neurons, muscle cells, or glands. Most presynaptic terminals in the central nervous system are formed along the axons (en passant boutons), not at their ends (terminal boutons).

Functionally, the axon terminal converts an electrical signal into a chemical signal. When an action potential arrives at an axon terminal (A), the neurotransmitter is released and diffuses across the synaptic cleft. If the postsynaptic cell (B) is also a neuron, neurotransmitter receptors generate a small electrical current that changes the postsynaptic potential. If the postsynaptic cell (B) is a muscle cell (neuromuscular junction), it contracts.

Upper motor neurons (UMNs) is a term introduced by William Gowers in 1886. They are found in the cerebral cortex and brainstem and carry information down to activate interneurons and lower motor neurons, which in turn directly signal muscles to contract or relax. UMNs represent the major origin point for voluntary somatic movement.

Upper motor neurons represent the largest pyramidal cells in the motor regions of the cerebral cortex. The major cell type of the UMNs is the Betz cells residing in layer V of the primary motor cortex, located on the precentral gyrus in the posterior frontal lobe. The cell bodies of Betz cell neurons are the largest in the brain, approaching nearly 0.1 mm in diameter. The axons of the upper motor neurons project out of the precentral gyrus travelling through to the brainstem, where they will decussate (intersect) within the lower medulla oblongata to form the lateral corticospinal tract on each side of the spinal cord. The fibers that do not decussate will pass through the medulla and continue on to form the anterior corticospinal tracts.

The enzyme cholinesterase (EC 3.1.1.8, choline esterase; systematic name acylcholine acylhydrolase) catalyses the hydrolysis of choline-based esters, several of which serve as neurotransmitters.:

These reactions are necessary to allow a cholinergic neuron to return to its resting state after activation. For example, in muscle contraction, acetylcholine at a neuromuscular junction triggers a contraction; but for the muscle to relax afterward, rather than remaining locked in a tense state, the acetylcholine must be broken down by a choline esterase.

Postsynaptic potentials are changes in the membrane potential of the postsynaptic terminal of a chemical synapse. Postsynaptic potentials are graded potentials, and should not be confused with action potentials although their function is to initiate or inhibit action potentials. Postsynaptic potentials occur when the presynaptic neuron releases neurotransmitters into the synaptic cleft. These neurotransmitters bind to receptors on the postsynaptic terminal, which may be a neuron, or a muscle cell in the case of a neuromuscular junction. These are collectively referred to as postsynaptic receptors, since they are located on the membrane of the postsynaptic cell. Postsynaptic potentials are important mechanisms by which neurons communicate with each other allowing for information processing, learning, memory formation, and complex behavior within the nervous system.

Myasthenia gravis (MG) is a long-term neuromuscular junction disease that leads to varying degrees of skeletal muscle weakness. The most commonly affected muscles are those of the eyes, face, and swallowing. It can result in double vision, drooping eyelids, and difficulties in talking and walking. Onset can be sudden. Those affected often have a large thymus or develop a thymoma.

Myasthenia gravis is an autoimmune disease of the neuromuscular junction which results from antibodies that block or destroy nicotinic acetylcholine receptors (AChR) at the junction between the nerve and muscle. This prevents nerve impulses from triggering muscle contractions. Most cases are due to immunoglobulin G1 (IgG1) and IgG3 antibodies that attack AChR in the postsynaptic membrane, causing complement-mediated damage and muscle weakness. Rarely, an inherited genetic defect in the neuromuscular junction results in a similar condition known as congenital myasthenia. Babies of mothers with myasthenia may have symptoms during their first few months of life, known as neonatal myasthenia or more specifically transient neonatal myasthenia gravis. Diagnosis can be supported by blood tests for specific antibodies, the edrophonium test, electromyography (EMG), or a nerve conduction study.