Characterizing the effects of Eugenol on neuronal ionic currents and hyperexcitability

Chin-Wei Huang, Julie Chi Chow, Jing Jane Tsai, Sheng-Nan Wu

研究成果: Article

24 引文 (Scopus)

摘要

Rationale: Eugenol (EUG, 4-allyl-2-methoxyphenol), the main component of essential oil extracted from cloves, has various uses in medicine because of its potential to modulate neuronal excitability. However, its effects on the ionic mechanisms remains incompletely understood. Objectives: We aimed to investigate EUG's effects on neuronal ionic currents and excitability, especially on voltage-gated ion currents, and to verify the effects on a hyperexcitability- temporal lobe seizure model. Methods: With the aid of patch-clamp technology, we first investigated the effects of EUG on ionic currents in NG108-15 neuronal cells differentiated with cyclic AMP. We then used modified Pinsky-Rinzel simulation modeling to evaluate its effects on spontaneous action potentials (APs). Finally, we investigated its effects on pilocarpine-induced seizures in rats. Results: EUG depressed the transient and late components of I Na in the neurons. It not only increased the degree of I Na inactivation, but specifically suppressed the non-inactivating I Na (I Na(NI)). Its inhibition of I Na(NI) was reversed by tefluthrin. In addition, EUG diminished L-type Ca 2+ current and delayed rectifier K + current only at higher concentrations. EUG's effects on APs frequency reduction was verified by the simulation modeling. In pilocarpine-induced seizures, the EUG-treated rats showed no shorter seizure latency but a lower seizure severity and mortality than the control rats. The EUG's effect on seizure severity was occluded by the I Na(NI) antagonist riluzole. Conclusion: The synergistic blocking effects of I Na and I Na(NI) contributes to the main mechanism through which EUG affects the firing of neuronal APs and modulate neuronal hyperexcitability such as pilocarpine-induced temporal lobe seizures.

原文English
頁(從 - 到)575-587
頁數13
期刊Psychopharmacology
221
發行號4
DOIs
出版狀態Published - 2012 六月 1

指紋

Eugenol
Seizures
Pilocarpine
Action Potentials
Temporal Lobe
Clove Oil
Riluzole
Volatile Oils
Cyclic AMP
Medicine
Ions
Technology
Neurons
Mortality

All Science Journal Classification (ASJC) codes

  • Pharmacology

引用此文

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abstract = "Rationale: Eugenol (EUG, 4-allyl-2-methoxyphenol), the main component of essential oil extracted from cloves, has various uses in medicine because of its potential to modulate neuronal excitability. However, its effects on the ionic mechanisms remains incompletely understood. Objectives: We aimed to investigate EUG's effects on neuronal ionic currents and excitability, especially on voltage-gated ion currents, and to verify the effects on a hyperexcitability- temporal lobe seizure model. Methods: With the aid of patch-clamp technology, we first investigated the effects of EUG on ionic currents in NG108-15 neuronal cells differentiated with cyclic AMP. We then used modified Pinsky-Rinzel simulation modeling to evaluate its effects on spontaneous action potentials (APs). Finally, we investigated its effects on pilocarpine-induced seizures in rats. Results: EUG depressed the transient and late components of I Na in the neurons. It not only increased the degree of I Na inactivation, but specifically suppressed the non-inactivating I Na (I Na(NI)). Its inhibition of I Na(NI) was reversed by tefluthrin. In addition, EUG diminished L-type Ca 2+ current and delayed rectifier K + current only at higher concentrations. EUG's effects on APs frequency reduction was verified by the simulation modeling. In pilocarpine-induced seizures, the EUG-treated rats showed no shorter seizure latency but a lower seizure severity and mortality than the control rats. The EUG's effect on seizure severity was occluded by the I Na(NI) antagonist riluzole. Conclusion: The synergistic blocking effects of I Na and I Na(NI) contributes to the main mechanism through which EUG affects the firing of neuronal APs and modulate neuronal hyperexcitability such as pilocarpine-induced temporal lobe seizures.",
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Characterizing the effects of Eugenol on neuronal ionic currents and hyperexcitability. / Huang, Chin-Wei; Chow, Julie Chi; Tsai, Jing Jane; Wu, Sheng-Nan.

於: Psychopharmacology, 卷 221, 編號 4, 01.06.2012, p. 575-587.

研究成果: Article

TY - JOUR

T1 - Characterizing the effects of Eugenol on neuronal ionic currents and hyperexcitability

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AU - Chow, Julie Chi

AU - Tsai, Jing Jane

AU - Wu, Sheng-Nan

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N2 - Rationale: Eugenol (EUG, 4-allyl-2-methoxyphenol), the main component of essential oil extracted from cloves, has various uses in medicine because of its potential to modulate neuronal excitability. However, its effects on the ionic mechanisms remains incompletely understood. Objectives: We aimed to investigate EUG's effects on neuronal ionic currents and excitability, especially on voltage-gated ion currents, and to verify the effects on a hyperexcitability- temporal lobe seizure model. Methods: With the aid of patch-clamp technology, we first investigated the effects of EUG on ionic currents in NG108-15 neuronal cells differentiated with cyclic AMP. We then used modified Pinsky-Rinzel simulation modeling to evaluate its effects on spontaneous action potentials (APs). Finally, we investigated its effects on pilocarpine-induced seizures in rats. Results: EUG depressed the transient and late components of I Na in the neurons. It not only increased the degree of I Na inactivation, but specifically suppressed the non-inactivating I Na (I Na(NI)). Its inhibition of I Na(NI) was reversed by tefluthrin. In addition, EUG diminished L-type Ca 2+ current and delayed rectifier K + current only at higher concentrations. EUG's effects on APs frequency reduction was verified by the simulation modeling. In pilocarpine-induced seizures, the EUG-treated rats showed no shorter seizure latency but a lower seizure severity and mortality than the control rats. The EUG's effect on seizure severity was occluded by the I Na(NI) antagonist riluzole. Conclusion: The synergistic blocking effects of I Na and I Na(NI) contributes to the main mechanism through which EUG affects the firing of neuronal APs and modulate neuronal hyperexcitability such as pilocarpine-induced temporal lobe seizures.

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