| Name | sodium channel (protein family or complex) |
|---|---|
| Synonyms | Sodium channel |
| Name | allethrin |
|---|---|
| CAS | 2-methyl-4-oxo-3-(2-propen-1-yl)-2-cyclopenten-1-yl 2,2-dimethyl-3-(2-methyl-1-propen-1-yl)cyclopropanecarboxylate |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 6286960 | Narahashi T: Modulation of nerve membrane channels by chemicals. J Physiol. 1981 May;77(9):1093-101. The tail current associated with step repolarization during the slow current in grayanotoxins decays with a dual exponential time course. 5. (+)-trans tetramethrin and (+)-trans allethrin also modify a fraction of sodium channel population in generating a slow current, which attains a maximum slowly and decays very slowly during a maintained depolarizing step. |
84(1,1,1,4) | Details |
| 6292640 | Abbassy MA, Eldefrawi ME, Eldefrawi AT: Allethrin interactions with the nicotinic acetylcholine receptor channel. Life Sci. 1982 Oct 11;31(15):1547-52. The high affinity binding of allethrin to the channel sites of the nicotinic -receptor may be indicative of a postsynaptic site of action for pyrethroids, in addition to their known action on the sodium channel. |
81(1,1,1,1) | Details |
| 8298967 | Ginsburg KS, Narahashi T: Differential sensitivity of tetrodotoxin-sensitive and tetrodotoxin-resistant channels to the insecticide allethrin in rat dorsal root ganglion neurons. Brain Res. 1993 Nov 12;627(2):239-48. In the tetrodotoxin-sensitive sodium channel currents, these changes caused by allethrin were much smaller or negligible. |
6(0,0,1,1) | Details |
| 1281937 | Narahashi T, Frey JM, Ginsburg KS, Roy ML: and -activated channels as the targets of pyrethroids and cyclodienes. Toxicol Lett. 1992 Dec;64-65 Spec No:429-36. The type I pyrethroid allethrin and the type II pyrethroid deltamethrin were both effective in prolonging the current in the TXX-resistant sodium channel but had only a small effect on the TTX-sensitive sodium channel. |
6(0,0,1,1) | Details |
| 2433987 | Narahashi T: Toxins that modulate the sodium channel gating mechanism. . Ann N Y Acad Sci. 1986;479:133-51. In the presence of type I pyrethroids which lack a cyano group at the alpha position (e.g., allethrin and tetramethrin), a large steady-state current appears during a step depolarization and a large slowly decaying tail current appears upon repolarization. |
5(0,0,0,5) | Details |
| 7854588 | Narahashi T, Roy ML, Ginsburg KS: Recent advances in the study of mechanism of action of marine neurotoxins. Neurotoxicology. 1994 Fall;15(3):545-54. The pyrethroid insecticide allethrin modifies tetrodotoxin-resistant channels while affecting tetrodotoxin-sensitive channels to a much lesser extent. Tetrodotoxin and saxitoxin block the sodium channel selectively without any effect on other types of voltage-activated and transmitter-activated ion channels. |
4(0,0,0,4) | Details |
| 1336116 | Gusovsky F, Padgett WL, Creveling CR, Daly JW: Interaction of pumiliotoxin B with an "alkaloid-binding domain" on the voltage-dependent sodium channel. Mol Pharmacol. 1992 Dec;42(6):1104-8. Both a type I pyrethroid (allethrin) and a type II pyrethroid (fenvalerate) inhibit PTX-B- and PTX-B/alpha-scorpion toxin-mediated 22Na+ influx. |
3(0,0,0,3) | Details |
| 19766671 | Breckenridge CB, Holden L, Sturgess N, Weiner M, Sheets L, Sargent D, Soderlund DM, Choi JS, Symington S, Clark JM, Burr S, Ray D: Evidence for a separate mechanism of toxicity for the Type I and the Type II pyrethroid insecticides. Neurotoxicology. 2009 Nov;30 Suppl 1:S17-31. Epub 2009 Sep 18. Neurotoxicity and mechanistic data were collected for six alpha-cyano pyrethroids (beta-cyfluthrin, cypermethrin, deltamethrin, esfenvalerate, fenpropathrin and lambda-cyhalothrin) and up to six non-cyano containing pyrethroids (bifenthrin, S-bioallethrin [or allethrin], permethrin, pyrethrins, resmethrin [or its cis-isomer, cismethrin] and tefluthrin under standard conditions. Factor analysis and multivariate dissimilarity analysis were employed to evaluate four independent data sets comprised of (1) fifty-six behavioral and physiological parameters from an acute neurotoxicity functional observatory battery (FOB), (2) eight electrophysiological parameters from voltage clamp experiments conducted on the Na (v) 1.8 sodium channel expressed in Xenopus oocytes, (3) indices of efficacy, potency and binding calculated for influx across neuronal membranes, membrane depolarization and released from rat brain synaptosomes and (4) changes in chloride channel open state probability using a patch voltage clamp technique for membranes isolated from mouse neuroblastoma cells. |
1(0,0,0,1) | Details |
| 6128164 | Narahashi T: Modification of nerve membrane channels by the insecticide pyrethroids. Comp Biochem Physiol C. 1982;72(2):411-4. The synthetic pyrethroids exert potent and selective actions on nerve membrane channels. (+)-trans tetramethrin and (+)-trans allethrin cause repetitive discharges to be produced in the isolated crayfish and squid giant axons in response to a single stimulus as a result of an increase in depolarizing after-potential. 2. The latter effect is due to slowing of the sodium channel kinetics which causes a prolonged current following the normal peak current. 3. |
2(0,0,0,2) | Details |
| 10989292 | Martin RL, Pittendrigh B, Liu J, Reenan R, ffrench-Constant R, Hanck DA: Point mutations in domain III of a Drosophila neuronal Na channel confer resistance to allethrin. Insect Biochem Mol Biol. 2000 Nov;30(11):1051-9. We screened several mutant sodium channel Drosophila lines for resistance to type I pyrethroids. |
1(0,0,0,1) | Details |
| 7780863 | Nozaki S, Takahashi M, Hashimoto K: Effect of pyrethroid (allethrin and fenvalerate) on excitability changes following nerve impulse. Sangyo Eiseigaku Zasshi. 1995 Jan;37(1):5-8. The difference has been reported to depend on the effect on the sodium channel opening time. |
1(0,0,0,1) | Details |
| 16180929 | Bradberry SM, Cage SA, Proudfoot AT, Vale JA: Poisoning due to pyrethroids. Toxicol Rev. 2005;24(2):93-106. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. The first pyrethroid pesticide, allethrin, was identified in 1949. |
1(0,0,0,1) | Details |
| 16051293 | Choi JS, Soderlund DM: Structure-activity relationships for the action of 11 pyrethroid insecticides on rat Na v 1.8 channels expressed in Xenopus oocytes. Toxicol Appl Pharmacol. 2006 Mar 15;211(3):233-44. Epub 2005 Jul 26. This paper describes the action of 11 structurally diverse commercial pyrethroid insecticides on the rat Na v 1.8 sodium channel isoform, the principal carrier of the tetrodotoxin-resistant, pyrethroid-sensitive current of sensory neurons, expressed in Xenopus laevis oocytes. All 11 compounds produced characteristic tail currents following a depolarizing pulse that ranged from rapidly-decaying monoexponential currents (allethrin, cismethrin and permethrin) to persistent biexponential currents (cyfluthrin, cyhalothrin, cypermethrin and deltamethrin). |
1(0,0,0,1) | Details |
| 2546657 | Gusovsky F, Secunda SI, Daly JW: Pyrethroids: involvement of channels in effects on formation in guinea pig synaptoneurosomes. Brain Res. 1989 Jul 17;492(1-2):72-8. Type II pyrethroids, like deltamethrin and fenvalerate, were more potent and, at least for deltamethrin, more efficacious than type I pyrethroids, like allethrin, resmethrin and permethrin. The effects of type II pyrethroids could be partially inhibited by the sodium channel blocker tetrodotoxin. |
1(0,0,0,1) | Details |
| 6276777 | Vijverberg HP, van der Zalm JM, van der Bercken J: Similar mode of action of pyrethroids and DDT on sodium channel gating in myelinated nerves. Nature. 1982 Feb 18;295(5850):601-3. |
1(0,0,0,1) | Details |
| 6302535 | Narahashi T: Cellular and molecular mechanisms of action of insecticides: neurophysiological approach. Neurobehav Toxicol Teratol. 1982 Nov-Dec;4(6):753-8. Type I pyrethroids as represented by allethrin and tetramethrin which lack a cyano group cause repetitive discharges in nerve fibers and nerve terminals leading to hyperexcitation of the animal. Thus, it is concluded that the site of action of pyrethroids is the sodium channel, and that pyrethroids interact with the channel macromolecules that control the gating mechanism. |
1(0,0,0,1) | Details |