The Experts below are selected from a list of 201 Experts worldwide ranked by ideXlab platform
Toshio Narahashi - One of the best experts on this subject based on the ideXlab platform.
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Single-channel analysis of Tetrodotoxin-sensitive and Tetrodotoxin-resistant sodium channels in rat dorsal root ganglion neurons
Brain research, 1994Co-Authors: Mary Louise Roy, Eitan Reuveny, Toshio NarahashiAbstract:Tetrodotoxin-sensitive and Tetrodotoxin-resistant single sodium channel currents were recorded from rat dorsal root ganglion neurons. The two types of sodium channel currents could be distinguished by the effects of predepolarization, 10 nM Tetrodotoxin, and the inactivation during depolarization. Single-channel conductances were calculated to be 6.3 and 3.4 pS in the Tetrodotoxin-sensitive and Tetrodotoxin-resistant channels, respectively.
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differential sensitivity of Tetrodotoxin sensitive and Tetrodotoxin resistant sodium channels to the insecticide allethrin in rat dorsal root ganglion neurons
Brain Research, 1993Co-Authors: Kenneth S. Ginsburg, Toshio NarahashiAbstract:The pyrethroid insecticides are known to modify neuronal sodium channels to cause a prolongation of whole cell current. The sodium channels expressed in the dorsal root ganglion neurons of the rat are of two types, one highly sensitive to Tetrodotoxin and the other highly resistant to Tetrodotoxin. The pyrethroid allethrin exerted profound effects on Tetrodotoxin-resistant sodium channels while causing minimal effects on Tetrodotoxin-sensitive sodium channels. Currents derived from Tetrodotoxin-resistant sodium channels were greatly prolonged during a step depolarization; the tail currents upon repolarization were also augmented and prolonged. In the Tetrodotoxin-sensitive sodium channel currents, these changes caused by allethrin were much smaller or negligible. The activation and inactivation voltages of Tetrodotoxin-resistant peak sodium currents were not significantly altered by allethrin. The differential action of allethrin on the two types of sodium channels would be important not only in identifying the target molecular structure but also in interpreting the symptoms of poisoning in mammals.
Laura Faravelli - One of the best experts on this subject based on the ideXlab platform.
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The anti-nociceptive agent ralfinamide inhibits Tetrodotoxin-resistant and Tetrodotoxin-sensitive Na+ currents in dorsal root ganglion neurons.
European journal of pharmacology, 2005Co-Authors: Tina C. Stummann, Patricia Salvati, Ruggero Fariello, Laura FaravelliAbstract:Abstract Tetrodotoxin-resistant and Tetrodotoxin-sensitive Na + channels contribute to the abnormal spontaneous firing in dorsal root ganglion neurons associated with neuropathic pain. Effects of the anti-nociceptive agent ralfinamide on Tetrodotoxin-resistant and Tetrodotoxin-sensitive currents in rat dorsal root ganglion neurons were therefore investigated by patch clamp experiments. Ralfinamide inhibition was voltage-dependent showing highest potency towards inactivated channels. IC 50 values for tonic block of half-maximal inactivated Tetrodotoxin-resistant and Tetrodotoxin-sensitive currents were 10 μM and 22 μM. Carbamazepine, an anticonvulsant used in the treatment of pain, showed significantly lower potency. Ralfinamide produced a hyperpolarising shift in the steady-state inactivation curves of both currents confirming the preferential interaction with inactivated channels. Additionally, ralfinamide use and frequency dependently inhibited both currents and significantly delayed repriming from inactivation. All effects were more pronounced for Tetrodotoxin-resistant than Tetrodotoxin-sensitive currents. The potency and mechanisms of actions of ralfinamide provide a hypothesis for the anti-nociceptive properties found in animal models.
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the anti nociceptive agent ralfinamide inhibits Tetrodotoxin resistant and Tetrodotoxin sensitive na currents in dorsal root ganglion neurons
European Journal of Pharmacology, 2005Co-Authors: Tina C. Stummann, Patricia Salvati, Ruggero Fariello, Laura FaravelliAbstract:Abstract Tetrodotoxin-resistant and Tetrodotoxin-sensitive Na + channels contribute to the abnormal spontaneous firing in dorsal root ganglion neurons associated with neuropathic pain. Effects of the anti-nociceptive agent ralfinamide on Tetrodotoxin-resistant and Tetrodotoxin-sensitive currents in rat dorsal root ganglion neurons were therefore investigated by patch clamp experiments. Ralfinamide inhibition was voltage-dependent showing highest potency towards inactivated channels. IC 50 values for tonic block of half-maximal inactivated Tetrodotoxin-resistant and Tetrodotoxin-sensitive currents were 10 μM and 22 μM. Carbamazepine, an anticonvulsant used in the treatment of pain, showed significantly lower potency. Ralfinamide produced a hyperpolarising shift in the steady-state inactivation curves of both currents confirming the preferential interaction with inactivated channels. Additionally, ralfinamide use and frequency dependently inhibited both currents and significantly delayed repriming from inactivation. All effects were more pronounced for Tetrodotoxin-resistant than Tetrodotoxin-sensitive currents. The potency and mechanisms of actions of ralfinamide provide a hypothesis for the anti-nociceptive properties found in animal models.
Jianmin Jiang - One of the best experts on this subject based on the ideXlab platform.
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Effects of (−)-Gallocatechin-3-Gallate on Tetrodotoxin-Resistant Voltage-Gated Sodium Channels in Rat Dorsal Root Ganglion Neurons
International journal of molecular sciences, 2013Co-Authors: Yan Zhang, Yan-yan Jia, Jin-lei Guo, Peiqing Liu, Jianmin JiangAbstract:The (−)-gallocatechin-3-gallate (GCG) concentration in some tea beverages can account for as much as 50% of the total catechins. It has been shown that catechins have analgesic properties. Voltage-gated sodium channels (Nav) mediate neuronal action potentials. Tetrodotoxin inhibits all Nav isoforms, but Nav1.8 and Nav1.9 are relatively Tetrodotoxin-resistant compared to other isoforms and functionally linked to nociception. In this study, the effects of GCG on Tetrodotoxin-resistant Na+ currents were investigated in rat primary cultures of dorsal root ganglion neurons via the whole-cell patch-clamp technique. We found that 1 μM GCG reduced the amplitudes of peak current density of Tetrodotoxin-resistant Na+ currents significantly. Furthermore, the inhibition was accompanied by a depolarizing shift of the activation voltage and a hyperpolarizing shift of steady-state inactivation voltage. The percentage block of GCG (1 μM) on Tetrodotoxin-resistant Na+ current was 45.1% ± 1.1% in 10 min. In addition, GCG did not produce frequency-dependent block of Tetrodotoxin-resistant Na+ currents at stimulation frequencies of 1 Hz, 2 Hz and 5 Hz. On the basis of these findings, we propose that GCG may be a potential analgesic agent.
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effects of gallocatechin 3 gallate on Tetrodotoxin resistant voltage gated sodium channels in rat dorsal root ganglion neurons
International Journal of Molecular Sciences, 2013Co-Authors: Yan Zhang, Yan-yan Jia, Jin-lei Guo, Peiqing Liu, Jianmin JiangAbstract:The (−)-gallocatechin-3-gallate (GCG) concentration in some tea beverages can account for as much as 50% of the total catechins. It has been shown that catechins have analgesic properties. Voltage-gated sodium channels (Nav) mediate neuronal action potentials. Tetrodotoxin inhibits all Nav isoforms, but Nav1.8 and Nav1.9 are relatively Tetrodotoxin-resistant compared to other isoforms and functionally linked to nociception. In this study, the effects of GCG on Tetrodotoxin-resistant Na+ currents were investigated in rat primary cultures of dorsal root ganglion neurons via the whole-cell patch-clamp technique. We found that 1 μM GCG reduced the amplitudes of peak current density of Tetrodotoxin-resistant Na+ currents significantly. Furthermore, the inhibition was accompanied by a depolarizing shift of the activation voltage and a hyperpolarizing shift of steady-state inactivation voltage. The percentage block of GCG (1 μM) on Tetrodotoxin-resistant Na+ current was 45.1% ± 1.1% in 10 min. In addition, GCG did not produce frequency-dependent block of Tetrodotoxin-resistant Na+ currents at stimulation frequencies of 1 Hz, 2 Hz and 5 Hz. On the basis of these findings, we propose that GCG may be a potential analgesic agent.
Tina C. Stummann - One of the best experts on this subject based on the ideXlab platform.
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The anti-nociceptive agent ralfinamide inhibits Tetrodotoxin-resistant and Tetrodotoxin-sensitive Na+ currents in dorsal root ganglion neurons.
European journal of pharmacology, 2005Co-Authors: Tina C. Stummann, Patricia Salvati, Ruggero Fariello, Laura FaravelliAbstract:Abstract Tetrodotoxin-resistant and Tetrodotoxin-sensitive Na + channels contribute to the abnormal spontaneous firing in dorsal root ganglion neurons associated with neuropathic pain. Effects of the anti-nociceptive agent ralfinamide on Tetrodotoxin-resistant and Tetrodotoxin-sensitive currents in rat dorsal root ganglion neurons were therefore investigated by patch clamp experiments. Ralfinamide inhibition was voltage-dependent showing highest potency towards inactivated channels. IC 50 values for tonic block of half-maximal inactivated Tetrodotoxin-resistant and Tetrodotoxin-sensitive currents were 10 μM and 22 μM. Carbamazepine, an anticonvulsant used in the treatment of pain, showed significantly lower potency. Ralfinamide produced a hyperpolarising shift in the steady-state inactivation curves of both currents confirming the preferential interaction with inactivated channels. Additionally, ralfinamide use and frequency dependently inhibited both currents and significantly delayed repriming from inactivation. All effects were more pronounced for Tetrodotoxin-resistant than Tetrodotoxin-sensitive currents. The potency and mechanisms of actions of ralfinamide provide a hypothesis for the anti-nociceptive properties found in animal models.
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the anti nociceptive agent ralfinamide inhibits Tetrodotoxin resistant and Tetrodotoxin sensitive na currents in dorsal root ganglion neurons
European Journal of Pharmacology, 2005Co-Authors: Tina C. Stummann, Patricia Salvati, Ruggero Fariello, Laura FaravelliAbstract:Abstract Tetrodotoxin-resistant and Tetrodotoxin-sensitive Na + channels contribute to the abnormal spontaneous firing in dorsal root ganglion neurons associated with neuropathic pain. Effects of the anti-nociceptive agent ralfinamide on Tetrodotoxin-resistant and Tetrodotoxin-sensitive currents in rat dorsal root ganglion neurons were therefore investigated by patch clamp experiments. Ralfinamide inhibition was voltage-dependent showing highest potency towards inactivated channels. IC 50 values for tonic block of half-maximal inactivated Tetrodotoxin-resistant and Tetrodotoxin-sensitive currents were 10 μM and 22 μM. Carbamazepine, an anticonvulsant used in the treatment of pain, showed significantly lower potency. Ralfinamide produced a hyperpolarising shift in the steady-state inactivation curves of both currents confirming the preferential interaction with inactivated channels. Additionally, ralfinamide use and frequency dependently inhibited both currents and significantly delayed repriming from inactivation. All effects were more pronounced for Tetrodotoxin-resistant than Tetrodotoxin-sensitive currents. The potency and mechanisms of actions of ralfinamide provide a hypothesis for the anti-nociceptive properties found in animal models.
Mary Louise Roy - One of the best experts on this subject based on the ideXlab platform.
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Single-channel analysis of Tetrodotoxin-sensitive and Tetrodotoxin-resistant sodium channels in rat dorsal root ganglion neurons
Brain research, 1994Co-Authors: Mary Louise Roy, Eitan Reuveny, Toshio NarahashiAbstract:Tetrodotoxin-sensitive and Tetrodotoxin-resistant single sodium channel currents were recorded from rat dorsal root ganglion neurons. The two types of sodium channel currents could be distinguished by the effects of predepolarization, 10 nM Tetrodotoxin, and the inactivation during depolarization. Single-channel conductances were calculated to be 6.3 and 3.4 pS in the Tetrodotoxin-sensitive and Tetrodotoxin-resistant channels, respectively.
