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Botulinum toxin, or botulinum neurotoxin (commonly called botox), is a neurotoxic protein produced by the bacterium Clostridium botulinum and related species. [24] It prevents the release of the neurotransmitter acetylcholine from axon endings at the neuromuscular junction , thus causing flaccid paralysis . [ 25 ]
Normally, these receptor channels allow sodium ions into muscle cells to initiate an action potential that leads to muscle contraction. By blocking the receptors, the neurotoxin is capable of significantly reducing neuromuscular junction signaling, an effect which has resulted in its use by anesthesiologists to produce muscular relaxation. [88]
Botulinum toxin: Inhibiting acetylcholine release 3–5 days 3–4 months Very potent; Botulinum poisoning cause parasympathetic and motor paralysis; Muscle relaxants Treat cervical dystonia, spasticity, blepharospasm and overactive bladder; Injected to paralyse muscles around face, hence reducing wrinkles (clinical or cosmetic uses) Reduce ...
The development of the neuromuscular junction requires signaling from both the motor neuron's terminal and the muscle cell's central region. During development, muscle cells produce acetylcholine receptors (AChRs) and express them in the central regions in a process called prepatterning.
The Clostridium botulinum bacteria are the cause of botulism. Vegetative cells of C. botulinum may be ingested. Introduction of the bacteria may also occur via endospores in a wound. When the bacteria are in vivo, they induce flaccid paralysis. This happens because C. botulinum produces a toxin that blocks the release of acetylcholine.
Along with some strains of Clostridium butyricum and Clostridium baratii, these bacteria all produce the toxin. [2] Botulinum toxin can cause botulism, a severe flaccid paralytic disease in humans and other animals, [3] and is the most potent toxin known to science, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg in humans. [4] [5]
The botulinum toxin has protease activity which degrades the SNAP-25 protein. The SNAP-25 protein is required for vesicle fusion that releases neurotransmitters, in particular acetylcholine. [ 23 ] Botulinum toxin essentially cleaves these SNARE proteins, and in doing so, prevents synaptic vesicles from fusing with the cellular synaptic ...
Botulinum toxin is a neurotoxin present in the cytoplasm of the anaerobic bacterium Clostridium botulinum. It binds presynaptically with high affinity to sites on cholinergic nerve terminals, decreasing release of acetylcholine , thereby blocking neuromuscular transmission, and causing flaccid muscle paralysis.