Effect of arvanil (N-arachidonoyl-vanillyl-amine), a nonpungent anandamide-capsaicin hybrid, on ion currents in NG108-15 neuronal cells

Yuk Keung Lo, Hung Ting Chiang, Sheng-Nan Wu

Research output: Contribution to journalArticle

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Abstract

The effects of arvanil (N-arachidonoyl-vanillyl-amine), a structural hybrid between capsaicin and anandamide, on ion currents in a mouse neuroblastoma and rat glioma hybrid cell line, NG108-15, were examined with the aid of the whole-cell voltage-clamp technique. Arvanil (0.2-50μM) caused an inhibition of voltage-dependent L-type Ca2+ current (ICa,L) in a concentration-dependent manner. Arvanil produced no change in the overall shape of the current-voltage relationship of ICa,L. The IC50 value of arvanil-induced inhibition of ICa,L was 2μM. Arvanil (5μM) could shift the steady-state inactivation curve of ICa,L to a more negative potential by approximately -15mV. No effect of arvanil (20μM) on delayed rectifier K+ current (IK(DR)) was observed; however, capsaicin (20μM), glyceryl nonivamide (20μM) and capsinolol (20μM) suppressed it significantly. Arvanil (20μM) caused a slight reduction in the amplitude of erg (ether-à-go-go-related)-mediated K+ current (IK(erg)) without modifying the activation curve of this current, while capsaicin and glyceryl nonivamide were more effective in suppressing IK(erg). Under current-clamp configuration, arvanil decreased the firing frequency of action potentials. Arvanil-mediated inhibition of ICa,L appeared to be independent of its binding to either vanilloid or cannabinoid receptors. The channel-blocking properties of arvanil may, at least in part, contribute to the underlying mechanisms by which it affects neuronal or neuroendocrine function.

Original languageEnglish
Pages (from-to)581-591
Number of pages11
JournalBiochemical Pharmacology
Volume65
Issue number4
DOIs
Publication statusPublished - 2003 Feb 15

Fingerprint

Capsaicin
Amines
Ions
Ether
Clamping devices
Electric potential
TRPV Cation Channels
Cannabinoid Receptors
Hybrid Cells
Patch-Clamp Techniques
Neuroblastoma
Glioma
Action Potentials
Inhibitory Concentration 50
Rats
Chemical activation
Cells
arvanil
anandamide
Cell Line

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

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title = "Effect of arvanil (N-arachidonoyl-vanillyl-amine), a nonpungent anandamide-capsaicin hybrid, on ion currents in NG108-15 neuronal cells",
abstract = "The effects of arvanil (N-arachidonoyl-vanillyl-amine), a structural hybrid between capsaicin and anandamide, on ion currents in a mouse neuroblastoma and rat glioma hybrid cell line, NG108-15, were examined with the aid of the whole-cell voltage-clamp technique. Arvanil (0.2-50μM) caused an inhibition of voltage-dependent L-type Ca2+ current (ICa,L) in a concentration-dependent manner. Arvanil produced no change in the overall shape of the current-voltage relationship of ICa,L. The IC50 value of arvanil-induced inhibition of ICa,L was 2μM. Arvanil (5μM) could shift the steady-state inactivation curve of ICa,L to a more negative potential by approximately -15mV. No effect of arvanil (20μM) on delayed rectifier K+ current (IK(DR)) was observed; however, capsaicin (20μM), glyceryl nonivamide (20μM) and capsinolol (20μM) suppressed it significantly. Arvanil (20μM) caused a slight reduction in the amplitude of erg (ether-{\`a}-go-go-related)-mediated K+ current (IK(erg)) without modifying the activation curve of this current, while capsaicin and glyceryl nonivamide were more effective in suppressing IK(erg). Under current-clamp configuration, arvanil decreased the firing frequency of action potentials. Arvanil-mediated inhibition of ICa,L appeared to be independent of its binding to either vanilloid or cannabinoid receptors. The channel-blocking properties of arvanil may, at least in part, contribute to the underlying mechanisms by which it affects neuronal or neuroendocrine function.",
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Effect of arvanil (N-arachidonoyl-vanillyl-amine), a nonpungent anandamide-capsaicin hybrid, on ion currents in NG108-15 neuronal cells. / Lo, Yuk Keung; Chiang, Hung Ting; Wu, Sheng-Nan.

In: Biochemical Pharmacology, Vol. 65, No. 4, 15.02.2003, p. 581-591.

Research output: Contribution to journalArticle

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AU - Lo, Yuk Keung

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N2 - The effects of arvanil (N-arachidonoyl-vanillyl-amine), a structural hybrid between capsaicin and anandamide, on ion currents in a mouse neuroblastoma and rat glioma hybrid cell line, NG108-15, were examined with the aid of the whole-cell voltage-clamp technique. Arvanil (0.2-50μM) caused an inhibition of voltage-dependent L-type Ca2+ current (ICa,L) in a concentration-dependent manner. Arvanil produced no change in the overall shape of the current-voltage relationship of ICa,L. The IC50 value of arvanil-induced inhibition of ICa,L was 2μM. Arvanil (5μM) could shift the steady-state inactivation curve of ICa,L to a more negative potential by approximately -15mV. No effect of arvanil (20μM) on delayed rectifier K+ current (IK(DR)) was observed; however, capsaicin (20μM), glyceryl nonivamide (20μM) and capsinolol (20μM) suppressed it significantly. Arvanil (20μM) caused a slight reduction in the amplitude of erg (ether-à-go-go-related)-mediated K+ current (IK(erg)) without modifying the activation curve of this current, while capsaicin and glyceryl nonivamide were more effective in suppressing IK(erg). Under current-clamp configuration, arvanil decreased the firing frequency of action potentials. Arvanil-mediated inhibition of ICa,L appeared to be independent of its binding to either vanilloid or cannabinoid receptors. The channel-blocking properties of arvanil may, at least in part, contribute to the underlying mechanisms by which it affects neuronal or neuroendocrine function.

AB - The effects of arvanil (N-arachidonoyl-vanillyl-amine), a structural hybrid between capsaicin and anandamide, on ion currents in a mouse neuroblastoma and rat glioma hybrid cell line, NG108-15, were examined with the aid of the whole-cell voltage-clamp technique. Arvanil (0.2-50μM) caused an inhibition of voltage-dependent L-type Ca2+ current (ICa,L) in a concentration-dependent manner. Arvanil produced no change in the overall shape of the current-voltage relationship of ICa,L. The IC50 value of arvanil-induced inhibition of ICa,L was 2μM. Arvanil (5μM) could shift the steady-state inactivation curve of ICa,L to a more negative potential by approximately -15mV. No effect of arvanil (20μM) on delayed rectifier K+ current (IK(DR)) was observed; however, capsaicin (20μM), glyceryl nonivamide (20μM) and capsinolol (20μM) suppressed it significantly. Arvanil (20μM) caused a slight reduction in the amplitude of erg (ether-à-go-go-related)-mediated K+ current (IK(erg)) without modifying the activation curve of this current, while capsaicin and glyceryl nonivamide were more effective in suppressing IK(erg). Under current-clamp configuration, arvanil decreased the firing frequency of action potentials. Arvanil-mediated inhibition of ICa,L appeared to be independent of its binding to either vanilloid or cannabinoid receptors. The channel-blocking properties of arvanil may, at least in part, contribute to the underlying mechanisms by which it affects neuronal or neuroendocrine function.

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