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Different G proteins mediate somatostatin‐induced inward rectifier K + currents in murine brain and endocrine cells
Author(s) -
Takano Koji,
YasufukuTakano Junko,
Kozasa Tohru,
Nakajima Shigehiro,
Nakajima Yasuko
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1997.559bj.x
Subject(s) - pertussis toxin , locus coeruleus , g protein , inward rectifier potassium ion channel , g alpha subunit , somatostatin , microbiology and biotechnology , endocrinology , alpha (finance) , medicine , biology , chemistry , protein subunit , signal transduction , biochemistry , receptor , central nervous system , ion channel , construct validity , nursing , gene , patient satisfaction
1 Types of G proteins (G protein α ‐subunit subtypes) which mediate the activation of inward rectifier K + currents by somatostatin (somatotrophin release‐inhibiting factor, SRIF) were determined in cultured locus coeruleus neurones from newborn rats and in AtT‐20 cells (a mouse pituitary cell line). 2 The whole‐cell patch clamp technique was used together with injection of antibodies against pertussis toxin (PTX)‐sensitive G protein α ‐subunits or with injection of antisense (or sense) oligonucleotides against these G proteins. 3 In locus coeruleus neurones, the SRIF‐induced activation of inward rectifier K + currents was inhibited by anti‐G α i1 /G α i2 antibody injection, but not by anti‐G α i3 or by anti‐G α o /G α i3 antibody injection, suggesting that the SRIF response is mediated through G α i1 and/or G α i2 . 4 The SRIF‐induced activation of the inward rectifier was suppressed in locus coeruleus neurones after injection of antisense oligonucleotides against G α i2 , but not by injection of sense oligonucleotides against G α i2 . Injection of antisense (or sense) oligonucleotides against G α i1 , G α i3 and G α o (common) had no effect. These results suggest that G α i2 is involved in this SRIF response. 5 In AtT‐20 cells, the SRIF‐induced activation of inward rectifier K + currents was suppressed by injection of anti‐G α i3 antibody, but not by injection of anti‐G α i1 /G α i2 antibody. 6 The above results indicate that G i mediates the SRIF effects on inward rectifier K + currents. However, different subtypes of G i are involved in the brain neurones and in the endocrine cells: G i2 in locus coeruleus neurones and G i3 in AtT‐20 cells.