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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]
A neuromuscular junction (or myoneural junction) is a chemical synapse between a motor neuron and a muscle fiber. [1] It allows the motor neuron to transmit a signal to the muscle fiber, causing muscle contraction. [2] Muscles require innervation to function—and even just to maintain muscle tone, avoiding atrophy.
Common examples of neurotoxins include lead, [7] ethanol (drinking alcohol), [8] glutamate, [9] nitric oxide, [10] botulinum toxin (e.g. Botox), [11] tetanus toxin, [12] and tetrodotoxin. [6] Some substances such as nitric oxide and glutamate are in fact essential for proper function of the body and only exert neurotoxic effects at excessive ...
By analyzing brain processes with acetylcholine, doctors can measure how much beta amyloid is around and use it to judge its effects on Alzheimer's. [11] Myasthenia gravis is an autoimmune disease, where the body produces antibodies targeted against the acetylcholine receptor on the postsynaptic membrane in the neuromuscular junction. Muscle ...
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: 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 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.
Botulinum toxins do not directly interact with SNAP, but indirectly impact its ability to assemble into the 20S complex leading to impaired synaptic transmission at the neuromuscular junction. The blocking of acetylcholine release onto the endplate leads to muscle paralysis and, if left untreated, death.