<b>Inhibition by capsaicin and its analogs of compound </b><b>action potentials in frog sciatic nerves </b>

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  • 坐骨神経の複合活動電位に対するカプサイシンとその類似物質の抑制作用

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It is well-known that capsaicin (Caps) activates TRPV1s existing in the peripheral and central terminals of primary-afferent fibers; the peripheral activation of TRPV1 produces action potentials and the central activation of TRPV1 leads to a barrage of the spontaneous release of L-glutamate from nerve terminals to spinal dorsal horn neurons. Although Caps was reported to produce a nerve conduction block, this action has not been thoroughly examined yet. We examined the actions of Caps and its analogs on Na+-channel blocker tetrodotoxin-sensitive and fast-conducting compound action potentials (CAPs) recorded from the frog sciatic nerve by use of the air-gap method.Caps reversibly reduced the peak amplitude of the CAP in a dose-dependent manner (by about 50% at 200 µM). Although a TRPV1 antagonist capsazepine (50 µM) by itself inhibited CAPs, this drug did not affect the Caps-induced inhibition of CAP. A TRPV1 agonist resiniferatoxin (5 µM) had no effect on CAPs. Caps analogs, dihydrocapsaicin, zingerone, eugenol and vanillin, also inhibited CAPs in a reversible and dose-dependent manner. A potency sequence of these inhibitions was Caps = dihydrocapsaicin > eugenol >> zingerone ≥ vanillin >> vanillylamine. Other Caps analog, vanillic acid, had almost no effect on CAPs. A TRPV1 agonist, olvanil, at 30 µM, a maximal concentration to dissolve this drug in Ringer solution, was less effective than was Caps in inhibiting CAPs. It is concluded that Caps inhibits CAPs without TRPV1 activation and that a chemical structure bound to the vanillyl group of Caps analogs plays a role in determining the extent of CAP inhibition. These results may serve to know molecular mechanisms for Caps-induced conduction block.

Journal

  • PAIN RESEARCH

    PAIN RESEARCH 24 (3), 159-167, 2009

    JAPANESE ASSOCIATION FOR STUDY OF PAIN

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