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Plant-derived chemicals including aroma oil compounds have an ability to inhibit nerve conduction and modulate transient receptor potential (TRP) channels. Although applying aroma oils to the skin produces a local anesthetic effect, this has not been yet examined throughly. The aim of the present study was to know how nerve conduction inhibitions by aroma oil compounds are related to their chemical structures and whether these activities are mediated by TRP activation. Compound action potentials (CAPs) were recorded from the frog sciatic nerve by using the air-gap method. Citral (aldehyde), which activates various types of TRP channels, attenuated the peak amplitude of CAP with the half-maximal inhibitory concentration (IC50) value of 0.46 mmol/L. Another aldehyde (citronellal), alcohol (citronellol, geraniol, (±)-linalool, (−)-linalool, (+)-borneol, (−)-borneol, α-terpineol), ester (geranyl acetate, linalyl acetate, bornyl acetate), and oxide (rose oxide) compounds also reduced CAP peak amplitudes (IC50: 0.50, 0.35, 0.53, 1.7, 2.0, 1.5, 2.3, 2.7, 0.51, 0.71, 0.44, and 2.6 mmol/L, respectively). On the other hand, the amplitudes were reduced by a small extent by hydrocarbons (myrcene and p-cymene) and ketone (camphor) at high concentrations (2–5 mmol/L). The activities of citral and other TRP agonists ((+)-borneol and camphor) were resistant to TRP antagonist ruthenium red. An efficacy sequence for the CAP inhibitions was generally aldehydes ≥ esters ≥ alcohols > oxides >> hydrocarbons. The CAP inhibition by the aroma oil compound was not related to its octanol–water partition coefficient. It is suggested that aroma oil compounds inhibit nerve conduction in a manner specific to their chemical structures without TRP activation.

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Although the application of aroma-oil compounds contained in plants such as lavender to the skin produces a local anesthetic effect, cellular mechanisms for this effect have not been fully examined yet. Since some of aroma oil-derived chemicals modulate transient receptor potential (TRP) channels expressed in primary-afferent neurons, this modulation may be involved in the local anesthetic effect. We have previously reported that plant-derived chemicals (capsaicin, menthol and allyl isothiocyanate, which activate TRPV1, TRPM8 and TRPA1 channels, respectively) at high concentrations inhibit fast-conducting and Na +-channel blocker tetrodotoxin-sensitive compound action potentials (CAPs) recorded from the frog sciatic nerve without TRP activation. The CAPs were also inhibited by opioids and adrenoceptor agonists without the activation of receptors for the agonists. The inhibitory actions were specific to their chemical structures. The present study examined how various aroma-oil compounds affect frog sciatic nerve CAPs by using the air-gap method. Lavender-oil compounds, linalyl acetate and linalool, reduced CAP peak amplitudes with the halfmaximal inhibitory concentration (IC50) values of 0.49 mM and 1.65 mM, respectively. When compared with local anesthetics' actions reported previously in the frog sciatic nerve, the linalyl acetate activity was similar to those of lidocaine, ropivacaine and cocaine (0.74, 0.34 and 0.80 mM, respectively), while the linalool one was comparable to that (2.2 mM) of procaine. Citral, which activated TRPV1, TRPM8, TRPA1 and TRPV3 channels, attenuated CAP peak amplitudes with the IC50 value of 0.48 mM ; this action was resistant to a non-selective TRP antagonist ruthenium red (0.3 mM). Camphor, a TRPV1 and TRPV3 agonist, also reduced CAP peak amplitudes (by 30％ at 5 mM) in a manner insensitive to ruthenium red. With respect to other aroma-oil compounds, citronellal and rose oxide reduced CAP peak amplitudes with the IC50 values of 0.50 mM and 2.0 mM, respectively, while myrcene at a high concentration such as 5 mM hardly reduced CAP peak amplitudes. Taking into consideration previously-reported frog sciatic nerve data, an efficacy sequence of aroma-oil compounds for the CAP