The Experts below are selected from a list of 201 Experts worldwide ranked by ideXlab platform
K. Kuschinsky - One of the best experts on this subject based on the ideXlab platform.
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in vivo microdialysis study of kavain on Veratridine induced glutamate release
European Journal of Pharmacology, 1998Co-Authors: Boris Ferger, Hanns Häberlein, Georg Boonen, K. KuschinskyAbstract:Abstract This is the first microdialysis study to address the effects of (±)-kavain on Veratridine-induced glutamate release in freely moving rats. (±)-Kavain (100 mg/kg, p.o.) significantly reduced Veratridine-induced glutamate release compared with that of vehicle-treated controls. Maximum extracellular glutamate levels were obtained 20–40 min after Veratridine stimulation (500 μM, added to the perfusate). In the control group the increase was 301% and in the (±)-kavain group the increase was significantly reduced to 219% (the basal value was 100%). These results demonstrate that (±)-kavain reduces Veratridine-induced glutamate release in vivo, which confirms previous in vitro data.
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In vivo microdialysis study of (+/-)-kavain on Veratridine-induced glutamate release.
European journal of pharmacology, 1998Co-Authors: Boris Ferger, Hanns Häberlein, Georg Boonen, K. KuschinskyAbstract:This is the first microdialysis study to address the effects of (+/-)-kavain on Veratridine-induced glutamate release in freely moving rats. (+/-)-Kavain (100 mg/kg, p.o.) significantly reduced Veratridine-induced glutamate release compared with that of vehicle-treated controls. Maximum extracellular glutamate levels were obtained 20-40 min after Veratridine stimulation (500 microM, added to the perfusate). In the control group the increase was 301% and in the (+/-)-kavain group the increase was significantly reduced to 219% (the basal value was 100%). These results demonstrate that (+/-)-kavain reduces Veratridine-induced glutamate release in vivo, which confirms previous in vitro data.
Noriyoshi Teramoto - One of the best experts on this subject based on the ideXlab platform.
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actions of Veratridine on tetrodotoxin sensitive voltage gated na currents nav1 6 in murine vas deferens myocytes
British Journal of Pharmacology, 2009Co-Authors: Hai Lei Zhu, Richard D. Wassall, Maki Takai, Hidetaka Morinaga, Masatoshi Nomura, Thomas C. Cunnane, Noriyoshi TeramotoAbstract:Background and purpose: The effects of Veratridine, an alkaloid found in Liliaceae plants, on tetrodotoxin (TTX)-sensitive voltage-gated Na+ channels were investigated in mouse vas deferens. Experimental approach: Effects of Veratridine on TTX-sensitive Na+ currents (INa) in vas deferens myocytes dispersed from BALB/c mice, homozygous mice with a null allele of NaV1.6 (NaV1.6−/−) and wild-type mice (NaV1.6+/+) were studied using patch-clamp techniques. Tension measurements were also performed to compare the effects of Veratridine on phasic contractions in intact tissues. Key results: In whole-cell configuration, Veratridine had a concentration-dependent dual action on the peak amplitude of INa: INa was enhanced by Veratridine (1–10 µM), while higher concentrations (≥30 µM) inhibited INa. Additionally, two membrane current components were evoked by Veratridine, namely a sustained inward current during the duration of the depolarizing rectangular pulse and a tail current at the repolarization. Although Veratridine caused little shift of the voltage dependence of the steady-state inactivation curve and the activation curve for INa, Veratridine enhanced a non-inactivating component of INa. Veratridine caused no detectable contractions in vas deferens from NaV1.6−/− mice, although in tissues from NaV1.6+/+ mice, Veratridine (≥3 µM) induced TTX-sensitive contractions. Similarly, no detectable inward currents were evoked by Veratridine in NaV1.6−/− vas deferens myocytes, while Veratridine elicited both the sustained and tail currents in cells taken from NaV1.6+/+ mice. Conclusions and implications: These results suggest that Veratridine possesses a dual action on INa and that the Veratridine-induced activation of contraction is induced by the activation of NaV1.6 channels.
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Actions of Veratridine on tetrodotoxin-sensitive voltage-gated Na+ currents, NaV1.6, in murine vas deferens myocytes.
British journal of pharmacology, 2009Co-Authors: Hai Lei Zhu, Richard D. Wassall, Maki Takai, Hidetaka Morinaga, Masatoshi Nomura, Thomas C. Cunnane, Noriyoshi TeramotoAbstract:Background and purpose: The effects of Veratridine, an alkaloid found in Liliaceae plants, on tetrodotoxin (TTX)-sensitive voltage-gated Na+ channels were investigated in mouse vas deferens. Experimental approach: Effects of Veratridine on TTX-sensitive Na+ currents (INa) in vas deferens myocytes dispersed from BALB/c mice, homozygous mice with a null allele of NaV1.6 (NaV1.6−/−) and wild-type mice (NaV1.6+/+) were studied using patch-clamp techniques. Tension measurements were also performed to compare the effects of Veratridine on phasic contractions in intact tissues. Key results: In whole-cell configuration, Veratridine had a concentration-dependent dual action on the peak amplitude of INa: INa was enhanced by Veratridine (1–10 µM), while higher concentrations (≥30 µM) inhibited INa. Additionally, two membrane current components were evoked by Veratridine, namely a sustained inward current during the duration of the depolarizing rectangular pulse and a tail current at the repolarization. Although Veratridine caused little shift of the voltage dependence of the steady-state inactivation curve and the activation curve for INa, Veratridine enhanced a non-inactivating component of INa. Veratridine caused no detectable contractions in vas deferens from NaV1.6−/− mice, although in tissues from NaV1.6+/+ mice, Veratridine (≥3 µM) induced TTX-sensitive contractions. Similarly, no detectable inward currents were evoked by Veratridine in NaV1.6−/− vas deferens myocytes, while Veratridine elicited both the sustained and tail currents in cells taken from NaV1.6+/+ mice. Conclusions and implications: These results suggest that Veratridine possesses a dual action on INa and that the Veratridine-induced activation of contraction is induced by the activation of NaV1.6 channels.
Boris Ferger - One of the best experts on this subject based on the ideXlab platform.
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in vivo microdialysis study of kavain on Veratridine induced glutamate release
European Journal of Pharmacology, 1998Co-Authors: Boris Ferger, Hanns Häberlein, Georg Boonen, K. KuschinskyAbstract:Abstract This is the first microdialysis study to address the effects of (±)-kavain on Veratridine-induced glutamate release in freely moving rats. (±)-Kavain (100 mg/kg, p.o.) significantly reduced Veratridine-induced glutamate release compared with that of vehicle-treated controls. Maximum extracellular glutamate levels were obtained 20–40 min after Veratridine stimulation (500 μM, added to the perfusate). In the control group the increase was 301% and in the (±)-kavain group the increase was significantly reduced to 219% (the basal value was 100%). These results demonstrate that (±)-kavain reduces Veratridine-induced glutamate release in vivo, which confirms previous in vitro data.
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In vivo microdialysis study of (+/-)-kavain on Veratridine-induced glutamate release.
European journal of pharmacology, 1998Co-Authors: Boris Ferger, Hanns Häberlein, Georg Boonen, K. KuschinskyAbstract:This is the first microdialysis study to address the effects of (+/-)-kavain on Veratridine-induced glutamate release in freely moving rats. (+/-)-Kavain (100 mg/kg, p.o.) significantly reduced Veratridine-induced glutamate release compared with that of vehicle-treated controls. Maximum extracellular glutamate levels were obtained 20-40 min after Veratridine stimulation (500 microM, added to the perfusate). In the control group the increase was 301% and in the (+/-)-kavain group the increase was significantly reduced to 219% (the basal value was 100%). These results demonstrate that (+/-)-kavain reduces Veratridine-induced glutamate release in vivo, which confirms previous in vitro data.
Hai Lei Zhu - One of the best experts on this subject based on the ideXlab platform.
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actions of Veratridine on tetrodotoxin sensitive voltage gated na currents nav1 6 in murine vas deferens myocytes
British Journal of Pharmacology, 2009Co-Authors: Hai Lei Zhu, Richard D. Wassall, Maki Takai, Hidetaka Morinaga, Masatoshi Nomura, Thomas C. Cunnane, Noriyoshi TeramotoAbstract:Background and purpose: The effects of Veratridine, an alkaloid found in Liliaceae plants, on tetrodotoxin (TTX)-sensitive voltage-gated Na+ channels were investigated in mouse vas deferens. Experimental approach: Effects of Veratridine on TTX-sensitive Na+ currents (INa) in vas deferens myocytes dispersed from BALB/c mice, homozygous mice with a null allele of NaV1.6 (NaV1.6−/−) and wild-type mice (NaV1.6+/+) were studied using patch-clamp techniques. Tension measurements were also performed to compare the effects of Veratridine on phasic contractions in intact tissues. Key results: In whole-cell configuration, Veratridine had a concentration-dependent dual action on the peak amplitude of INa: INa was enhanced by Veratridine (1–10 µM), while higher concentrations (≥30 µM) inhibited INa. Additionally, two membrane current components were evoked by Veratridine, namely a sustained inward current during the duration of the depolarizing rectangular pulse and a tail current at the repolarization. Although Veratridine caused little shift of the voltage dependence of the steady-state inactivation curve and the activation curve for INa, Veratridine enhanced a non-inactivating component of INa. Veratridine caused no detectable contractions in vas deferens from NaV1.6−/− mice, although in tissues from NaV1.6+/+ mice, Veratridine (≥3 µM) induced TTX-sensitive contractions. Similarly, no detectable inward currents were evoked by Veratridine in NaV1.6−/− vas deferens myocytes, while Veratridine elicited both the sustained and tail currents in cells taken from NaV1.6+/+ mice. Conclusions and implications: These results suggest that Veratridine possesses a dual action on INa and that the Veratridine-induced activation of contraction is induced by the activation of NaV1.6 channels.
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Actions of Veratridine on tetrodotoxin-sensitive voltage-gated Na+ currents, NaV1.6, in murine vas deferens myocytes.
British journal of pharmacology, 2009Co-Authors: Hai Lei Zhu, Richard D. Wassall, Maki Takai, Hidetaka Morinaga, Masatoshi Nomura, Thomas C. Cunnane, Noriyoshi TeramotoAbstract:Background and purpose: The effects of Veratridine, an alkaloid found in Liliaceae plants, on tetrodotoxin (TTX)-sensitive voltage-gated Na+ channels were investigated in mouse vas deferens. Experimental approach: Effects of Veratridine on TTX-sensitive Na+ currents (INa) in vas deferens myocytes dispersed from BALB/c mice, homozygous mice with a null allele of NaV1.6 (NaV1.6−/−) and wild-type mice (NaV1.6+/+) were studied using patch-clamp techniques. Tension measurements were also performed to compare the effects of Veratridine on phasic contractions in intact tissues. Key results: In whole-cell configuration, Veratridine had a concentration-dependent dual action on the peak amplitude of INa: INa was enhanced by Veratridine (1–10 µM), while higher concentrations (≥30 µM) inhibited INa. Additionally, two membrane current components were evoked by Veratridine, namely a sustained inward current during the duration of the depolarizing rectangular pulse and a tail current at the repolarization. Although Veratridine caused little shift of the voltage dependence of the steady-state inactivation curve and the activation curve for INa, Veratridine enhanced a non-inactivating component of INa. Veratridine caused no detectable contractions in vas deferens from NaV1.6−/− mice, although in tissues from NaV1.6+/+ mice, Veratridine (≥3 µM) induced TTX-sensitive contractions. Similarly, no detectable inward currents were evoked by Veratridine in NaV1.6−/− vas deferens myocytes, while Veratridine elicited both the sustained and tail currents in cells taken from NaV1.6+/+ mice. Conclusions and implications: These results suggest that Veratridine possesses a dual action on INa and that the Veratridine-induced activation of contraction is induced by the activation of NaV1.6 channels.
Koei Ojima - One of the best experts on this subject based on the ideXlab platform.
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excitatory mechanism of Veratridine on slowly adapting pulmonary stretch receptors in anesthetized rabbits
Life Sciences, 1998Co-Authors: Shigeji Matsumoto, Chikako Saiki, Takeshi Tanimoto, Mamoru Takeda, Toshiaki Takahashi, Koei OjimaAbstract:The excitatory effects of Veratridine on slowly adapting pulmonary stretch receptors (SARs) were studied before and after administration of ouabain (a Na+-K+ ATPase inhibitor) in anesthetized, artificially ventilated rabbits after vagus nerve section. Administration of Veratridine (40 μgkg) stimulated SAR activity but did not significantly alter tracheal pressure. Administration of ouabain (50 μgkg) initially stimulated SAR activity during both inflation and deflation, but after 20 min, two different types of SAR responses were observed; one became silent at the peak, of inflation only, and the other maintained excitatory activity during both inflation and deflation phases. Veratridine usually inhibited SAR activity in ouabain-treated animals, irrespective of the difference of ouabain effects. These results suggest that Veratridine-induced stimulation of SARs is closely related to the change in the Na+ ion gradient, which is regulated by Na+ pump activity.
