Traditional Japanese medicines inhibit compound action potentials in the frog sciatic nerve

Matsushita, Akitomo; Fujita, Teizo; Ohtsubo, Satoshi; Kumamoto, Eiichi

doi:10.1016/j.jep.2015.12.018

Cited by 11 publications

(7 citation statements)

References 56 publications

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“…The conduction velocity of the fibers averaged 26±2 m/s (range: 16–49 m/s; n =28). These values were comparable to those reported previously [14] , [26] , [29] , [30] , [31] , [32] , [33] , [34] , [35] . DMSO at 1% (the maximal concentration used in the present study) did not affect CAPs; the peak amplitude of the CAP was 106±2% of control (taken as 100%; 32.2±3.5 mV; n =4) ( p >0.05), 20 min after treatment with DMSO.…”

Section: Resultssupporting

confidence: 92%

“…The efficacy of BPA was similar to those of pramoxine, ropivacaine and levobupivacaine (0.21, 0.34 and 0.23 mM, respectively), higher than those of prilocaine, procaine, lidocaine and cocaine (IC 50 =1.8, 2.3, 0.74 and 0.80 mM, respectively), and lower than that of tetracaine (0.014 mM). Many plant-derived chemicals have been reported to inhibit frog sciatic nerve CAPs with efficacies similar to those of LAs [26] , [31] , [33] , [34] , [35] . Further study is required to clarify the interaction between BPA and LA receptor sites on Na + channels.…”

Section: Discussionmentioning

confidence: 99%

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Bisphenol A inhibits compound action potentials in the frog sciatic nerve in a manner independent of estrogen receptors

Mizuta

Fujita

Yamagata

et al. 2017

Biochemistry and Biophysics Reports

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Although the endocrine disruptor bisphenol A (BPA) is reported to inhibit nerve conduction, the underlying mechanisms are unclear. Therefore, in the present study, we examined the effect of BPA on compound action potentials (CAPs) recorded from the frog sciatic nerve using the air-gap method. Treatment of the sciatic nerve with BPA (0.5 mM) for 20 min reduced the peak amplitude of the CAP by approximately 60% in a partially reversible manner. The reduction in the CAP peak amplitude was concentration-dependent, with a half-maximal inhibitory concentration (IC50) value of 0.31 mM. This effect of BPA was unaffected by an estrogen-receptor antagonist, 4-hydroxytamoxifen, which by itself reduced CAP peak amplitude, with an IC50 value of 0.26 mM (comparable to that of BPA). The natural estrogen 17β-estradiol, at the highest dissolvable concentration (0.05 mM), had an effect similar to that of BPA. The IC50 value of BPA was comparable to those of some local anesthetics in inhibiting frog CAPs. Our findings suggest that BPA inhibits nerve conduction in a manner independent of estrogen receptors. This action of BPA may underlie, at least in part, the neurotoxicity of the compound.

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Section: Resultssupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Bisphenol A inhibits compound action potentials in the frog sciatic nerve in a manner independent of estrogen receptors

Mizuta

Fujita

Yamagata

et al. 2017

Biochemistry and Biophysics Reports

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“…With respect to the activities of three kinds of crude medicine contained in daikenchuto, CAPs were inhibited by Japanese pepper and processed ginger while being hardly affected by ginseng radix. Japanese pepper's IC 50 value was 0.77 mg/mL and the extent of CAP peak amplitude reduction produced by processed ginger at 2 mg/mL was 31% [290]. At least a part of Kampo medicine's antinociceptive effect could attribute to its nerve AP conduction inhibitory action.…”

Section: Antinociceptive Plant-derived Compounds Inhibit Nerve Conducmentioning

confidence: 92%

Inhibition of Fast Nerve Conduction Produced by Analgesics and Analgesic Adjuvants—Possible Involvement in Pain Alleviation

Kumamoto

2020

Pharmaceuticals

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Nociceptive information is transmitted from the periphery to the cerebral cortex mainly by action potential (AP) conduction in nerve fibers and chemical transmission at synapses. Although this nociceptive transmission is largely inhibited at synapses by analgesics and their adjuvants, it is possible that the antinociceptive drugs inhibit nerve AP conduction, contributing to their antinociceptive effects. Many of the drugs are reported to inhibit the nerve conduction of AP and voltage-gated Na+ and K+ channels involved in its production. Compound action potential (CAP) is a useful measure to know whether drugs act on nerve AP conduction. Clinically-used analgesics and analgesic adjuvants (opioids, non-steroidal anti-inflammatory drugs, α2-adrenoceptor agonists, antiepileptics, antidepressants and local anesthetics) were found to inhibit fast-conducting CAPs recorded from the frog sciatic nerve by using the air-gap method. Similar actions were produced by antinociceptive plant-derived chemicals. Their inhibitory actions depended on the concentrations and chemical structures of the drugs. This review article will mention the inhibitory actions of the antinociceptive compounds on CAPs in frog and mammalian peripheral (particularly, sciatic) nerves and on voltage-gated Na+ and K+ channels involved in AP production. Nerve AP conduction inhibition produced by analgesics and analgesic adjuvants is suggested to contribute to at least a part of their antinociceptive effects.

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“…The former two have been shown to suppress CAPs while the last has no effects on CAPs. Japanese pepper had an IC 50 value of 0.77 mg/mL, and processed ginger at a concentration of 2 mg/mL reduced the peak amplitudes of CAPs by 31% [326]. A small part of the analgesic effect of Kampo medicine may be due to its nerve AP conduction inhibitory action.…”

Section: Actions Of Plant-derived Compounds On Nerve Ap Conductionmentioning

confidence: 99%

Inhibitory Actions of Clinical Analgesics, Analgesic Adjuvants, and Plant-Derived Analgesics on Nerve Action Potential Conduction

Kumamoto

2022

Encyclopedia

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The action potential (AP) conduction in nerve fibers plays a crucial role in transmitting nociceptive information from the periphery to the cerebral cortex. Nerve AP conduction inhibition possibly results in analgesia. It is well-known that many analgesics suppress nerve AP conduction and voltage-dependent sodium and potassium channels that are involved in producing APs. The compound action potential (CAP) recorded from a bundle of nerve fibers is a guide for knowing if analgesics affect nerve AP conduction. This entry mentions the inhibitory effects of clinically used analgesics, analgesic adjuvants, and plant-derived analgesics on fast-conducting CAPs and voltage-dependent sodium and potassium channels. The efficacies of their effects were compared among the compounds, and it was revealed that some of the compounds have similar efficacies in suppressing CAPs. It is suggested that analgesics-induced nerve AP conduction inhibition may contribute to at least a part of their analgesic effects.

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Traditional Japanese medicines inhibit compound action potentials in the frog sciatic nerve

Cited by 11 publications

References 56 publications

Bisphenol A inhibits compound action potentials in the frog sciatic nerve in a manner independent of estrogen receptors

Bisphenol A inhibits compound action potentials in the frog sciatic nerve in a manner independent of estrogen receptors

Inhibition of Fast Nerve Conduction Produced by Analgesics and Analgesic Adjuvants—Possible Involvement in Pain Alleviation

Inhibitory Actions of Clinical Analgesics, Analgesic Adjuvants, and Plant-Derived Analgesics on Nerve Action Potential Conduction

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