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Manipulation of the delayed rectifier Kv1.5 potassium channel in glial cells by antisense oligodeoxynucleotides
Author(s) -
Roy Mary Louise,
Saal Daniel,
Perney Teresa,
Sontheimer Harald,
Waxman Stephen G.,
Kaczmarek Leonard K.
Publication year - 1996
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199611)18:3<177::aid-glia2>3.0.co;2-x
Subject(s) - potassium channel , biology , neuroglia , inward rectifier potassium ion channel , potassium channel blocker , spinal cord , hippocampal formation , astrocyte , microbiology and biotechnology , patch clamp , tetraethylammonium , neuroscience , electrophysiology , biophysics , central nervous system , ion channel , biochemistry , chemistry , potassium , receptor , organic chemistry
Glial cells have been shown to express several biophysically and pharmacology distinct potassium channel types. However, the molecular identity of most glial K + channels is unknown. We have developed an antibody specific for the Shaker type potassium channel Kv1.5 protein, and demonstrate by immunohistochemistry the presence of this channel in glial cells of adult rat hippocampal and cerebellar slices, as well as in cultured spinal cord astrocytes. Immunoreactivity was particularly intense in the endfoot processes of astrocytes surrounding the microvasculature of the hippocampus. The specific contribution of this channel protein to the delayed rectifying K + current of spinal cord astrocytes was determined by incubating these cells with antisense oligodeoxynucleotides complementary to the mRNA coding for Kv1.5 protein. Such treatment reduced delayed rectifier current density and shifted the potassium current steady‐state inactivation, without altering current activation, cell capacitance, or cell resting potential. The tetraethylammonium acetate (TEA) sensitivity of astrocytic delayed rectifier current was enhanced following antisense oligodeoxynucleotide treatment, suggesting that Kv1.5 channel protein may provide a significant component of the TEA‐insensitive current in this preparation. Our results suggest that Kv1.5 is widely expressed in glial cells of brain and spinal cord and that delayed rectifying K + currents in astrocytes are largely mediated by Kv1.5 channel protein. © 1996 Wiley‐Liss, Inc.