The toxin Tx4(6-1) from the spider Phoneutria nigriventer slows down Na + current inactivation in insect CNS via binding to receptor site 3

Tx4(6-1) a neurotoxic peptide from the venom of the aggressive South American ‘armed’ spider Phoneutria nigriventer, has been previously isolated and sequenced. It shows no detectable activity in mice but affects the peripheral nervous system of insects by stimulating glutamate release at the neurom...

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Bibliographic Details
Published in:Journal of insect physiology 2002, Vol.48 (1), p.53-61
Main Authors: de Lima, M.E, Stankiewicz, M, Hamon, A, de Figueiredo, S.G, Cordeiro, M.N, Diniz, C.R, Martin-Eauclaire, M.-F, Pelhate, M
Format: Article
Language:English
Subjects:
Insect
Neurotoxin
Sodium channel
Spider
α-Toxin
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Summary:Tx4(6-1) a neurotoxic peptide from the venom of the aggressive South American ‘armed’ spider Phoneutria nigriventer, has been previously isolated and sequenced. It shows no detectable activity in mice but affects the peripheral nervous system of insects by stimulating glutamate release at the neuromuscular junction. Here we investigate possible interactions of the toxin with voltage-activated sodium channels (Na v). We confirm that it is ineffective on mammalian Na v channels, and establish that it competes with the α-like toxin 125 I -Bom IV, for binding on the site 3 of insect Na v channel (IC 50 value around 25 nM). The physiological consequences of this binding to the insect Na v channel are shown by electrophysiology: Tx4(6-1) prolongs evoked axonal action potentials (APs) (
ISSN:0022-1910
1879-1611
DOI:10.1016/S0022-1910(01)00143-3