AUTHOR=Du Yixing , Kiyoshi Conrad M. , Wang Qi , Wang Wei , Ma Baofeng , Alford Catherine C. , Zhong Shiying , Wan Qi , Chen Haijun , Lloyd Eric E. , Bryan Robert M. Jr. , Zhou Min 

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

JOURNAL=Frontiers in Cellular Neuroscience

VOLUME=10

YEAR=2016

URL=https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2016.00013

DOI=10.3389/fncel.2016.00013

ISSN=1662-5102

ABSTRACT=<p>We have recently shown that a linear current-to-voltage (I-V) relationship of membrane conductance (passive conductance) reflects the intrinsic property of K<sup>+</sup> channels in mature astrocytes. While passive conductance is known to underpin a highly negative and stable membrane potential (<italic>V</italic><sub>M</sub>) essential for the basic homeostatic function of astrocytes, a complete repertoire of the involved K<sup>+</sup> channels remains elusive. TREK-1 two-pore domain K<sup>+</sup> channel (K<sub>2P</sub>) is highly expressed in astrocytes, and covalent association of TREK-1 with TWIK-1, another highly expressed astrocytic K<sub>2P</sub>, 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<sup>+</sup> channels, such as K<sub>ir</sub>4.1, K<sub>ir</sub>5.1, and TREK-2, was not altered in these gene knockout mice. Whole-cell recording from hippocampal astrocytes <italic>in situ</italic> revealed no detectable changes in astrocyte passive conductance, <italic>V</italic><sub>M</sub>, or membrane input resistance (<italic>R</italic><sub>in</sub>) 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<sup>+</sup> channels may shed light on this long-standing and important question in astrocyte physiology.</p>