Research Papers:
Potential independent action of sigma receptor ligands through inhibition of the Kv2.1 channel
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Abstract
Xinying Liu1,*, Yingmei Fu2,3,*, Huan Yang2, Timur Mavlyutov2,4, Jun Li2,5, Christopher R. McCurdy6, Lian-Wang Guo2,7,8 and Bikash R. Pattnaik7,9
1Departments of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
2Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
3Shanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China
4Department of Anesthesiology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
5Department of Ophthalmology, The Third People’s Hospital of Dalian, Dalian, PR China
6Department of Medicinal Chemistry, College of Pharmacy, University of Florida, Gainesville, FL, USA
7McPherson Eye Research Institute, University of Wisconsin, Madison, WI, USA
8Department of Surgery and Department of Physiology & Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, USA
9Department of Pediatrics, Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
*These authors have contributed equally to this work
Correspondence to:
Bikash R. Pattnaik, email: [email protected]
Lian-Wang Guo, email: [email protected]
Keywords: Kv2.1 channel, CRISPR/Cas9, sigma receptor ligands, patch-clamp, electroretinogram
Received: April 21, 2017 Accepted: June 16, 2017 Published: July 26, 2017
ABSTRACT
The sigma-1 receptor (σ1-R) and sigma-2 receptor (σ2-R) are potential drug targets for treatment of cancer, pain, depression, retinal degeneration and other neuronal diseases. Previous reports show that sigma-1 receptor modulates the activities of multiple channels. We are interested in possible sigma receptor modulation of Kv2.1, a K+ channel abundant in retinal photoreceptors. We tested the effect of established sigma receptor ligands on Kv2.1 channels which were stably expressed in HEK293 cells. Surprisingly, σ1-R antagonists inhibited Kv2.1 currents in both wild type and σ1-R knockout HEK293 cells that we engineered using the CRISPR/Cas9 technology. Moreover, PB28, a σ1-R antagonist and also σ2-R agonist, inhibited Kv2.1 in σ1-R knockout cells, but this action was not blocked by the σ2-R antagonists that did not have an effect on Kv2.1. We also observed inhibition of electroretinogram by PB28 in wild type as well as σ1-R knockout mice. Thus, the results in this study indicate that the Kv2.1-inhibiting function of the sigma ligands is not sigma receptor dependent, suggesting a direct effect of these ligands on the Kv2.1 channel.
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