Original Article

Metergoline inhibits the neuronal Nav1.2 voltage-dependent Na+ channels expressed in Xenopus oocytes

Jun-ho Lee, Jian Liu, Minkyu Shin, Moochang Hong, Seung-yeol Nah, Hyunsu Bae
DOI: 10.1038/aps.2014.30

Abstract

Jun-ho LEE1, §, #, Jian LIU1, #, Minkyu SHIN1, Moochang HONG1, Seung-yeol NAH2, Hyunsu BAE1, *
1Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul 130–701, Republic of Korea; 2College of Veterinary Medicine, Konkuk University, Seoul 130–701, Republic of Korea

Aim: Metergoline is an ergot-derived psychoactive drug that acts as a ligand for serotonin and dopamine receptors. The aim of this study was to investigate the regulatory effects of metergoline on the neuronal Nav1.2 voltage-dependent Na+ channels in vitro.
Methods: Xenopus oocytes were injected with cRNAs encoding rat brain Nav1.2 α and β1 subunits. Voltage-activated Na+ currents were recorded using two-electrode voltage clamp technique. Drugs were applied though perfusion.

Results: Both metergoline and lidocaine reversibly and concentration-dependently inhibited the peak of Na+ currents with IC50 values of 3.6±4.2 and 916.9±98.8 μmol/L, respectively. Metergoline (3 μmol/L) caused a 6.8±1.2 mV depolarizing shift of the steady-state activation curve of the Na+ currents, and did not alter the inactivation curve. In contrast, lidocaine (3 μmol/L) caused a 12.7±1.2 mV hyperpolarizing shift of the inactivation curve of the Na+ currents without changing the steady-state activation curve. Both metergoline and lidocaine produced tonic and use-dependent inhibition on the peak of Na+ currents.

Conclusion: Metergoline exerts potent inhibition on the activity of neuronal Nav1.2 channels, which may contribute to its actions on the central nervous system.


Keywords: metergoline; ergot alkaloid; antidepressant; Na+ channels; Nav1.2; Xenopus oocyte; lidocaine

This work was supported by a National Research Foundation of Korea (NRF) Grant funded by the Korean government (MEST) (No 2011-006220).
§ Present address: Duke University Medical Center, Durham, NC 27710, USA.
# These authors contributed equally to this work.
* To whom correspondence should be addressed.
E-mail hbae@khu.ac.kr
Received 2014-02-11 Accepted 2014-03-21
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