Next Article in Journal
Site-Directed Mutagenesis of the Fibronectin Domains in Insulin Receptor-Related Receptor
Next Article in Special Issue
Analgesic Mechanisms of Antidepressants for Neuropathic Pain
Previous Article in Journal
Genome-Wide Development of MicroRNA-Based SSR Markers in Medicago truncatula with Their Transferability Analysis and Utilization in Related Legume Species
Previous Article in Special Issue
Antidepressants and Mood Stabilizers: Novel Research Avenues and Clinical Insights for Bipolar Depression
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2017, 18(11), 2460;

Activation of TREK-1, but Not TREK-2, Channel by Mood Stabilizers

Department of Physiology, College of Medicine and Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Korea
Author to whom correspondence should be addressed.
Received: 13 October 2017 / Revised: 14 November 2017 / Accepted: 16 November 2017 / Published: 19 November 2017
Full-Text   |   PDF [1107 KB, uploaded 19 November 2017]   |  


Earlier studies have demonstrated that the tandem pore domain weak inward rectifying K+ channel (TWIK)-related K+ (TREK)-1 channel is inhibited by antidepressants and is associated with major depression. However, little is known about the effect of mood stabilizers that are commonly used for treatment of bipolar disorder on TREK channels, members of the two-pore domain K+ (K2P) channel family. This study sought to investigate the effect of mood stabilizers on TREK-1 and TREK-2 channels. HEK-293A cells were transfected with human TREK-1 or TREK-2 DNA. The effect of mood stabilizers on TREK-1 and TREK-2 was studied using the patch clamp technique. Changes in TREK protein expression by mood stabilizers were studied in the HT-22 mouse hippocampal neuronal cells using western blot analysis. Lithium chloride (LiCl, 1 mM), gabapentin (100 μM), valproate (100 μM), and carbamazepine (100 μM) increased TREK-1 currents by 31 ± 14%, 25 ± 11%, 28 ± 12%, and 72 ± 12%, respectively, whereas they had no effect on TREK-2 channel activity. In addition, western blot analysis showed LiCl and carbamazepine slightly upregulated TREK-1 expression, but not TREK-2 in the HT-22 cells. These results suggest that TREK-1 could be a potential therapeutic target for treatment of bipolar disorders as well as depression, while TREK-2 is a target well suited for treatment of major depression. View Full-Text
Keywords: bipolar disorders; depression; mood stabilizers; tandem pore domain potassium channels bipolar disorders; depression; mood stabilizers; tandem pore domain potassium channels

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Kim, E.-J.; Lee, D.K.; Hong, S.-G.; Han, J.; Kang, D. Activation of TREK-1, but Not TREK-2, Channel by Mood Stabilizers. Int. J. Mol. Sci. 2017, 18, 2460.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top