Abstract
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.
Highlights
Nociceptive information from the periphery to the cerebral cortex is mainly transmitted by action potential (AP) conduction in nerve fibers and chemical transmission at synapses
non-steroidal anti-inflammatory drugs (NSAIDs), which are more effective in frog sciatic nerve Compound action potential (CAP) inhibition compared to the other NSAIDs [21], have two benzene rings that bind a hydrophilic substituent group, both of which rings are linked by -NH, as seen in local anesthetics
The CAPs are fast-conducting TTX-sensitive Aα fiber-mediated ones, nociceptive information is transmitted by slow-conducting Aδ and C fibers [1]
Summary
Nociceptive information from the periphery to the cerebral cortex is mainly transmitted by action potential (AP) conduction in nerve fibers and chemical transmission at synapses (see [1,2] for reviews). Frog sciatic nerve fast-conducting CAPs were found to be inhibited by clinically-used antinociceptive drugs such as many kinds of opioids including tramadol [19,20], NSAIDs [21], an α2-adrenoceptor agonist dexmedetomidine ((+)-(S)-4-[1-(2,3-dimethylphenyl)-ethyl]-1H-imidazole or DEX [22]), antiepileptics [23], antidepressants [24] and many kinds of local anesthetics (lidocaine, ropivacaine, prilocaine, levobupivacaine, bupivacaine, cocaine, procaine, benzocaine, tetracaine and pramoxine [19,20,23,25,26,27]) and by a general anesthetic propofol [25] These inhibitory actions were concentration-dependent and depended on the chemical structures of the drugs. It will be shown that antinociceptive plant-derived compounds inhibit frog sciatic nerve CAPs with efficacies comparable to those of NSAIDs and analgesic adjuvants
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