(biochemistry) A neurotoxin elaborated by the bacterium Clostridium tetani and which is responsible for the manifestations of tetanus.
Tetanospasmin
| Sci-Tech Dictionary: tetanospasmin |
(′tet·ən·ō′spaz·mən)
| 5min Related Video: Tetanospasmin |
| Medical Dictionary: tet·a·no·spas·min |
(tĕt'n-ō-spăz'mĭn)
n.
n.
The neurotoxin of Clostridium tetani that causes the characteristic signs and symptoms of tetanus.
| Veterinary Dictionary: tetanospasmin |
The neurotoxic exotoxin produced by Clostridium tetani, which inhibits release of gamma amino butyric acid by inhibitory neurons, resulting in tetanic spasms.
| Wikipedia: Tetanospasmin |
Tetanospasmin is the neurotoxin produced by the vegetative cell of Clostridium tetani[1] in anaerobic conditions, causing tetanus. It has no known function for clostridia in the soil environment where they are normally encountered. It is sometimes called spasmogenic toxin, tetanus toxin or abbreviated to TeTx or TeNT.
C. tetani also produces the exotoxin tetanolysin, the effects of which are as yet unclear.
The genes encoding these toxin are located on separate plasmids within the bacterium.
Contents |
Distribution
Tetanospasmin spreads through tissue spaces into the lymphatic and vascular systems. It enters the nervous system at the neuromuscular junctions and migrates through nerve trunks and into the central nervous system (CNS) by retrograde axonal transport.[2]>[3]
Structure
The protein tetanospasmin has a molecular weight of 150kDa. It is made up of two parts: a 100kDa heavy or B-chain and a 50kDa light or A-chain. The chains are connected by a disulfide bond.
- The B-chain binds to disialogangliosides (GD2 and GD1b) on the neuronal membrane.
- The A-chain, a zinc endopeptidase, attacks the vesicle-associated membrane protein (VAMP).
Function
The action of the A-chain stops the affected neurons from releasing the inhibitory neurotransmitters GABA (gamma-aminobutyric acid) and glycine by degrading the protein synaptobrevin.[4] The consequence of this is dangerous overactivity in the muscles from the smallest stimulus—the failure of inhibition of motor reflexes by sensory stimulation. This causes generalized contractions of the agonist and antagonist musculature, termed a tetanic spasm.
Clinical significance
Tetanic spasms can occur in a distinctive form called opisthotonos and be sufficiently severe to fracture long bones. The shorter nerves are the first to be inhibited, which leads to the characteristic early symptoms in the face and jaw, risus sardonicus and lockjaw.
The toxin bind to the neurons is irreversible[2] and nerve function can only be returned by the growth of new terminals and synapses. Tetanospasmin is used to create the toxoid used in immunization, such as the childhood DTP vaccine.
References
- ^ tetanospasmin at Dorland's Medical Dictionary
- ^ a b Farrar JJ; Yen LM; Cook T; Fairweather N; Binh N; Parry J; Parry CM (September 2000). "Tetanus". Journal of Neurology, Neurosurgery, and Psychiatry 69 (3): 292–301. PMID 10945801.
- ^ AU Lalli G; Gschmeissner S; Schiavo G (November 15, 2003). "Myosin Va and microtubule-based motors are required for fast axonal retrograde transport of tetanus toxin in motor neurons". Journal of Cell Science 116 (22): 4639–50. PMID 14576357.
- ^ Schiavo G; Benfenati F; Poulain B; Rossetto O; Polverino de Laureto P; DasGupta BR; Montecucco C (October 29, 1992). "Tetanus and botulinum-B neurotoxins block neurotransmitter release by proteolytic cleavage of synaptobrevin". Nature 359 (6398): 832–5. PMID 1331807.
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 | tetanus |
| Clostridium tetani (medicine) |
| toxin |
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