Interactions of tetramethrin, fenvalerate and DDT at the sodium channel in rat dorsal root ganglion neurons

Song, Jin-Ho; Nagata, Keiichi; Tatebayashi, Hideharu; Narahashi, Toshio

doi:10.1016/0006-8993(95)01239-7

Cited by 58 publications

(33 citation statements)

References 18 publications

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“…The hooked tail currents induced by deltamethrin in this study have been observed in mammalian neurons and sodium channels expressed in oocytes (such as Lund and Narahashi, 1982;Vijverberg et al, 1982;Song et al, 1996;Vais et al, 2000). The initial increasing phase of the tail current is the result of the delayed closing of the inactivation gate upon termination of depolarization.…”

Section: Discussionsupporting

confidence: 57%

“…Specifically, the sodium current during depolarization is prolonged, and the tail current associated with repolarization is greatly augmented. The pyrethroid-induced tail current has been used to quantify pyrethroid modification of the sodium channel (Lund and Narahashi, 1982;Vijverberg et al, 1982;Song et al, 1996;Lee et al, 1999c;Vais et al, 2000). Cohen and colleagues (Vais et al, 2000) compared two tail current recording protocols, one with a 500 ms depolarization from −100 to 0 mV and the other with a 100-pulse train of 5 ms depolarization from −100 to 0 mV.…”

Section: Kdr-type Mutations Altered the Para Csma Channel Sensitivitymentioning

confidence: 99%

“…For example, both DDT and pyrethroid insecticides, although structurally different, cause repetitive discharge or nerve membrane depolarization by modifying sodium channel gating (references in Narahashi, 1988;Soderlund and Bloomquist, 1989). Results from electrophysiological (such as Narahashi, 1988;Takeda and Narahashi, 1988;Song et al, 1996) and pharmacological studies (such as Jacques et al, 1980, Bloomquist andSoderlund, 1988;Brown et al, 1988;Lombet et al, 1988;Trainer et al, 1997) suggest a distinct receptor site(s) for pyrethroids. Although the electrophysiological effects of pyrethroids on sodium channels have been well-defined, our understanding of the molecular interactions between sodium channels and pyrethroids remains rudimentary.…”

Section: Introductionmentioning

confidence: 99%

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Novel sodium channel gene mutations in Blattella germanica reduce the sensitivity of expressed channels to deltamethrin

Tan

Liu

Tsai³

et al. 2002

Insect Biochemistry and Molecular Biology

104

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Pyrethroid insecticides alter the normal gating of voltage-gated sodium channels in the nervous system. Three sodium channel mutations (E434K, C764R, L993F) were recently identified in pyrethroid resistant German cockroach populations. In this report, we show that the L993F mutation decreased sodium channel sensitivity to the pyrethroid, deltamethrin, by five-fold in Xenopus oocytes. In contrast, neither E434K nor C764R alone decreased channel sensitivity to deltamethrin. However, E434K or C764R combined with L993F reduced deltamethrin sensitivity by 100-fold. Furthermore, concomitant presence of all three mutations (KRF) reduced channel sensitivity to deltamethrin by 500-fold. None of the mutations significantly affected channel gating. However, sodium current amplitudes from the mutant sodium channel carrying either E434K or C764R alone were much reduced compared to those of the wild-type channel or the channel carrying the double or triple mutations (KF, RF and KRF). These results indicated that evolution of sodium channel insensitivity in the German cockroach is achieved by sequential selection of a primary mutation L993F and two secondary mutations E434K and C764R, and concomitant presence of all three mutations dramatically reduced sodium channel sensitivity to deltamethrin.

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Section: Discussionsupporting

confidence: 57%

Section: Kdr-type Mutations Altered the Para Csma Channel Sensitivitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Novel sodium channel gene mutations in Blattella germanica reduce the sensitivity of expressed channels to deltamethrin

Tan

Liu

Tsai³

et al. 2002

Insect Biochemistry and Molecular Biology

104

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“…In TTX-R sodium channels, fenvalerate, a type II pyrethroid, irreversibly prolongs the sodium current during depolarization and greatly augments and prolongs the tail current (26). We previously demonstrated that the intrathecal (i.t.)…”

mentioning

confidence: 99%

Effect of Mexiletine on Fenvalerate-Induced Nociceptive Response in Diabetic Mice

2004

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Abstract. The effect of mexiletine on the nociceptive behavior induced by the intrathecal injection of fenvalerate, which predominantly activates tetrodotoxin-resistant (TTX-R) sodium channels, was studied in diabetic mice. The intrathecal injection of fenvalerate induced a characteristic behavioral syndrome that mainly consisted of reciprocal hind limb scratching directed toward caudal parts of the body and biting or licking of the hind legs in mice. The intensity of fenvalerate-induced nociceptive responses was significantly greater in diabetic mice than non-diabetic mice. This fenvalerate-induced behavior was dose-dependently inhibited by mexiletine (3 -30 mg / kg, i.p.). Intrathecal pretreatment with fenvalerate produced thermal hyperalgesia and allodynia in the tail-flick test in naive mice. Furthermore, mexiletine at doses of 10 and 30 mg / kg, i.p., dose-dependently and significantly reduced fenvalerate-induced thermal hyperalgesia and allodynia in the tail-flick test in naive mice. These present data suggest that i.p. pretreatment with mexiletine produced dose-dependent inhibition of fenvalerate-induced hyperalgesia and allodynia in mice, especially diabetic mice. This effect may be, at least in part, mediated by the inhibition of TTX-R sodium channel-mediated nociceptive transmission in the spinal cord.

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“…In TTX-R sodium channels, fenvalerate, a type II pyrethroid, irreversibly prolongs the sodium current during depolarization and greatly augments and prolongs the tail current (24).…”

mentioning

confidence: 99%

Nociception and Allodynia/Hyperalgesia Induced by Intrathecal Administration of Fenvalerate

Kamei

Sasaki²,

Zushida

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-The intrathecal injection of fenvalerate, a sodium channel activator, at doses of 0.01 to 3 mg, dose-dependently induced the duration of a characteristic behavioral syndrome mainly consisting of reciprocal hind limb scratching directed towards caudal parts of the body and biting or licking of the hind legs in mice. Fenvalerate-induced behavior was inhibited by morphine (1 -10 mg/ kg, i.p.). The characteristic behavior was also inhibited by mexiletine, a sodium channel blocker; MK-801, a N-methyl-D-aspartate ionchannel blocker; and GR82334, a neurokinin-1-receptor antagonist. Calphostin C (3 pmol, i.t.), a protein kinase C inhibitor, inhibited fenvalerate-induced behavior. On the other hand, phorbol-12, 13-dibutyrate (50 pmol, i.t.), a protein kinase C activator, markedly enhanced the fenvalerate-induced behavior. The present results also showed that fenvalerate produced thermal allodynia and hyperalgesia in the tail-flick test. Furthermore, fenvalerate-induced thermal allodynia and hyperalgesia were inhibited by the pretreatment with calphostin C. These results suggest that the intrathecal administration of fenvalerate induces a marked nociceptive response and thermal allodynia/ hyperalgesia, and they suggest that tetrodotoxin-resistant sodium channels may play an important role in this effect.Keywords: Allodynia, Hyperalgesia, Nociception, Fenvalerate, Tetrodotoxin-resistant sodium channelOpening of voltage-gated sodium channels causes a rapid depolarization of the membrane potential and constitutes the upstroke phase of the action potential. Most neuronal sodium channels can be blocked by tetrodotoxin (TTX) with Kd values of 1 -10 nM. However, sodium channels that are resistant to the blocking action of TTX have been found in both the central and peripheral nervous systems (1 -3). Dorsal root ganglion neurons express a slow activating and inactivating TTX-resistant (TTX-R) sodium channel as well as a fast activating and inactivating TTX-sensitive (TTX-S) sodium channel (4 -7). The TTX-R sodium channel is predominantly expressed in the capsaicin-sensitive small neurons of the dorsal root ganglion and appears to play an important role in nociceptive transmission (8 -13), and especially in allodynia and hyperalgesia (14). Furthermore, algogenic mediators such as prostaglandin, adenosine and serotonin enhance TTX-R sodium current (15 -17). Null mutant mice for TTX-R sodium channels show antinociception in response to noxious mechanical stimuli and a delayed development of inflammatory hyperalgesia (18). In spinal cord astrocytes, protein kinase C enhanced TTX-R sodium channels with leftward shifts in the voltagedependence of both activation and inactivation and produced faster kinetics (19). Several studies using protein kinase Cg-knockout mice (20) and diabetic animals (21 -23) have indicated that protein kinase C may play important roles in hyperalgesia.The pyrethroid insecticides are known to modulate the gating kinetics of neuronal sodium channels to cause repetitive discharges and membrane depolariza...

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Interactions of tetramethrin, fenvalerate and DDT at the sodium channel in rat dorsal root ganglion neurons

Cited by 58 publications

References 18 publications

Novel sodium channel gene mutations in Blattella germanica reduce the sensitivity of expressed channels to deltamethrin

Novel sodium channel gene mutations in Blattella germanica reduce the sensitivity of expressed channels to deltamethrin

Effect of Mexiletine on Fenvalerate-Induced Nociceptive Response in Diabetic Mice

Nociception and Allodynia/Hyperalgesia Induced by Intrathecal Administration of Fenvalerate

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