Abstract:
:Tetanus neurotoxin and botulinum neurotoxins are the causative agents of tetanus and botulism. They block the release of neurotransmitters from synaptic vesicles in susceptible animals and man and act in nanogram quantities because of their ability to specifically attack motoneurons. They developed an ingenious strategy to enter neurons. This involves a concentration step via complex polysialo gangliosides at the plasma membrane and the uptake and ride in recycling synaptic vesicles initiated by binding to a specific protein receptor. Finally, the neurotoxins shut down the synaptic vesicle cycle, which they had misused before to enter their target cells, via specific cleavage of protein core components of the cellular membrane fusion machinery. The uptake of four out of seven known botulinum neurotoxins into synaptic vesicles has been demonstrated to rely on binding to intravesicular segments of the synaptic vesicle proteins synaptotagmin or synaptic vesicle protein 2. This review summarizes the present knowledge about the cell receptor molecules and the mode of toxin-receptor interaction that enables the toxins' sophisticated access to their site of action.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Binz T,Rummel Adoi
10.1111/j.1471-4159.2009.06093.xsubject
Has Abstractpub_date
2009-06-01 00:00:00pages
1584-95issue
6eissn
0022-3042issn
1471-4159pii
JNC6093journal_volume
109pub_type
杂志文章,评审abstract::The effects of acute and chronic administration of buspirone, a serotonin 5-HT1A agonist, on the 5-HT synthesis rates in various rat brain structures were investigated using alpha-[14C]methyl-L-tryptophan (alpha-[14C]MTrp) and an autoradiographic method. In the acute treatment study, buspirone (10 mg/kg) was injected ...
journal_title:Journal of neurochemistry
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doi:10.1046/j.1471-4159.1999.0722022.x
更新日期:1999-05-01 00:00:00
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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doi:10.1046/j.1471-4159.2002.01060.x
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:1986-04-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1983.tb04804.x
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pub_type: 杂志文章
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更新日期:2004-01-01 00:00:00
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journal_title:Journal of neurochemistry
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更新日期:2004-05-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1046/j.1471-4159.1994.63062365.x
更新日期:1994-12-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1985.tb05554.x
更新日期:1985-10-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1983.tb08133.x
更新日期:1983-06-01 00:00:00
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journal_title:Journal of neurochemistry
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pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1986.tb00676.x
更新日期:1986-09-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:2015-05-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1046/j.1471-4159.1995.65031007.x
更新日期:1995-09-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:1996-11-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:2004-10-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1046/j.1471-4159.1996.67020880.x
更新日期:1996-08-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1992.tb11331.x
更新日期:1992-04-01 00:00:00
abstract::Vitamin A metabolite retinoic acid (RA) plays a major role in the aging adult brain plasticity. Conversely, chronic excess of glucocorticoids (GC) elicits some deleterious effects in the hippocampus. We questioned here the involvement of RA and GC in the expression of target proteins in hippocampal neurons. We investi...
journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/jnc.12192
更新日期:2013-05-01 00:00:00
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pub_type: 杂志文章
doi:10.1111/j.1471-4159.1992.tb09323.x
更新日期:1992-01-01 00:00:00