Neuromuscular junction in the context of "Motor innervation"

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Neuromuscular junction in the context of Motor neuron

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 neuronupper 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.

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Neuromuscular junction in the context of Chemical synapse

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.

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Neuromuscular junction in the context of Botulinum toxin

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.

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Neuromuscular junction in the context of Leg braces

Orthotics (Greek: Ορθός, romanizedortho, 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.

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Neuromuscular junction in the context of Asthenia

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.

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Neuromuscular junction in the context of Muscular weakness

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".

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Neuromuscular junction in the context of Nicotinic acetylcholine receptor

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.)

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Neuromuscular junction in the context of Double vision

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.

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