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Modulation of divalent cation‐activated chloride ion currents
Author(s) -
Scott R.H.,
McGuirk S.M.,
Dolphin A.C.
Publication year - 1988
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1988.tb11572.x
Subject(s) - divalent , extracellular , biophysics , chemistry , gtp' , calcium , pertussis toxin , g protein , intracellular , caffeine , biochemistry , endocrinology , biology , receptor , enzyme , organic chemistry
1 Voltage‐sensitive calcium channel currents carried by Ca 2+ (I Ca ) or Ba 2+ (I Ba ) were followed by tail currents carried by Cl − ions in approximately 45% of cultured dorsal root ganglion neurones. 2 Extracellular application of (−)‐baclofen (100 μm) inhibited I Ba and I Cl(Ba) BaY K 8644 (5 μm) potentiated both currents. 3 Intracellular GTP‐γ‐S increased the proportion of neurones in which I Cl(Ba) was recorded. In addition, the activation by GTP‐γ‐S of a pertussis toxin‐sensitive GTP binding (G)‐protein resulted in a steady increase in the Cl − tail current with time, despite a concurrent reduction in I Ba . 4 Extracellular application of 10 mM caffeine selectively reduced I Cl(Ba) without significant change in I Ba . When Ca 2+ was the charge carrier, caffeine had little effect on I Cl(Ca) , and increased the inactivation of I Ca . 5 We conclude that, in addition to being regulated by divalent cation entry through Ca 2+ channels, the Cl − current is also regulated by G‐protein activation. The mechanism of activation of I Cl(Ba) may involve Ca 2+ release from intracellular stores.