Document Report Card

ID: ALA2203149

Journal: J Nat Prod

Title: Carvacrol decreases neuronal excitability by inhibition of voltage-gated sodium channels.

Authors: Joca HC, Cruz-Mendes Y, Oliveira-Abreu K, Maia-Joca RP, Barbosa R, Lemos TL, Lacerda Beirão PS, Leal-Cardoso JH.

Abstract: The monoterpenoid carvacrol (1) is present in many essential oils of plants and has attracted attention because of its beneficial biological activities, especially analgesic activity. However, the mechanism of action of 1 remains unknown. The present study aimed to explore the mechanisms whereby 1 produces its effects on the peripheral nervous system. Carvacrol reversibly blocked the excitability of the rat sciatic nerve in a concentration-dependent manner with an IC(50) value of 0.50 ± 0.04 mM. At 0.6 mM, 1 increased the rheobase from 3.30 ± 0.06 V to 4.16 ± 0.14 V and the chronaxy from 59.6 ± 1.22 μs to 75.0 ± 1.82 μs. Also, 1 blocked the generation of action potentials (IC(50) 0.36 ± 0.14 mM) of the intact dorsal root ganglion (DRG) neurons without altering the resting potential and input resistance. Carvacrol reduced the voltage-gated sodium current of dissociated DRG neurons (IC(50) 0.37 ± 0.05 mM). In this study it has been demonstrated that 1 blocks neuronal excitability by a direct inhibition of the voltage-gated sodium current, which suggests that this compound acts as a local anesthetic. The present findings add valuable information to help understand the mechanisms implicated in the analgesic activity of carvacrol.

CiteXplore: 22967040

DOI: 10.1021/np300050g