Key result
Thyrotropin-releasing hormone significantly reduced the maximal available erg current amplitude by 12% (erg1), 13% (erg2), and 39% (erg3) in GH3/B6 cells.
Population
Clonal somatomammotroph GH3/B6 cells injected with cDNA coding for rat erg1, erg2, erg3 and HERG K+ channels
Design
Preclinical
Authors
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May modulate pituitary and cardiac excitability; leaves open translational relevance to human HERG-related arrhythmias.
TRH modulates all three members of the erg channel subfamily (including HERG) in GH3/B6 cells via an unidentified signaling pathway.
Schledermann et al. (2001) studied this question. Thyrotropin-releasing hormone (TRH) was evaluated on erg K+ current modulation. Thyrotropin-releasing hormone significantly reduced the maximal available erg current amplitude by 12% (erg1), 13% (erg2), and 39% (erg3) in GH3/B6 cells.
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