title: Genetic Deletion of TREK-1 or TWIK-1/TREK-1 Potassium Channels does not Alter the Basic Electrophysiological Properties of Mature Hippocampal Astrocytes In Situ.
abstract: We have recently shown that a linear current-to-voltage (I-V) relationship of membrane conductance (passive conductance) reflects the intrinsic property of K(+) channels in mature astrocytes. While passive conductance is known to underpin a highly negative and stable membrane potential (V M) essential for the basic homeostatic function of astrocytes, a complete repertoire of the involved K(+) channels remains elusive. TREK-1 two-pore domain K(+) channel (K2P) is highly expressed in astrocytes, and covalent association of TREK-1 with TWIK-1, another highly expressed astrocytic K2P, has been reported as a mechanism underlying the trafficking of heterodimer TWIK-1/TREK-1 channel to the membrane and contributing to astrocyte passive conductance. To decipher the individual contribution of TREK-1 and address whether the appearance of passive conductance is conditional to the co-expression of TWIK-1/TREK-1 in astrocytes, TREK-1 single and TWIK-1/TREK-1 double gene knockout mice were used in the present study. The relative quantity of mRNA encoding other astrocyte K(+) channels, such as Kir4.1, Kir5.1, and TREK-2, was not altered in these gene knockout mice. Whole-cell recording from hippocampal astrocytes in situ revealed no detectable changes in astrocyte passive conductance, V M, or membrane input resistance (R in) in either kind of gene knockout mouse. Additionally, TREK-1 proteins were mainly located in the intracellular compartments of the hippocampus. Altogether, genetic deletion of TREK-1 alone or together with TWIK-1 produced no obvious alteration in the basic electrophysiological properties of hippocampal astrocytes. Thus, future research focusing on other K(+) channels may shed light on this long-standing and important question in astrocyte physiology.
authors: Department of Neuroscience, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Department of Neurology, The First Affiliated Hospital of Nanjing Medical UniversityNanjing, China.
authors: Yixing
authors: Y
authors: Du
authors: Department of Neuroscience, The Ohio State University Wexner Medical Center Columbus, OH, USA.
authors: Conrad M
authors: CM
authors: Kiyoshi
authors: Department of Neuroscience, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Department of Neurology, Meitan General HospitalXibahe Nanli, Beijing, China.
authors: Qi
authors: Q
authors: Wang
authors: Department of Physiology, Institute of Brain Research, School of Basic Medicine, Huazhong University of Science and Technology Wuhan, China.
authors: Wei
authors: W
authors: Wang
authors: Department of Neuroscience, The Ohio State University Wexner Medical Center Columbus, OH, USA.
authors: Baofeng
authors: B
authors: Ma
authors: Department of Neuroscience, The Ohio State University Wexner Medical Center Columbus, OH, USA.
authors: Catherine C
authors: CC
authors: Alford
authors: Department of Neuroscience, The Ohio State University Wexner Medical Center Columbus, OH, USA.
authors: Shiying
authors: S
authors: Zhong
authors: Department of Neurology, The First Affiliated Hospital of Nanjing Medical University Nanjing, China.
authors: Qi
authors: Q
authors: Wan
authors: Department of Biological Science, University at Albany, State University of New York Albany, NY, USA.
authors: Haijun
authors: H
authors: Chen
authors: Department of Anesthesiology, Baylor College of Medicine Houston, TX, USA.
authors: Eric E
authors: EE
authors: Lloyd
authors: Department of Anesthesiology, Baylor College of Medicine Houston, TX, USA.
authors: Robert M
authors: RM
authors: Bryan
authors: Department of Neuroscience, The Ohio State University Wexner Medical Center Columbus, OH, USA.
authors: Min
authors: M
authors: Zhou
keywords: TREK-1 potassium channel; astrocytes; hippocampus; passive membrane conductance; patch-clamp recording