Vol. 278, Issue 3, E430-E443, March 2000
Contribution of changes in the chloride driving force to the
fading of IGABA in frog melanotrophs
Frank
le Foll,
Olivier
Soriani,
Hubert
Vaudry, and
Lionel
Cazin
European Institute for Peptide Research (Institut
Fédératif de Recherches Multidisciplinaires sur les
Peptides no. 23), Laboratory of Cellular and Molecular
Neuroendocrinology, Institut National de la Santé et de la
Recherche Médicale Unité 413, Unité Associée au
Centre National de la Recherche Scientifique, University of Rouen,
76821 Mont-Saint-Aignan, France
Chloride redistribution during type A 
-aminobutyric
acid (GABAA) currents (IGABA) has been
investigated in cultured frog pituitary melanotrophs with imposed
intracellular chloride concentration ([Cl
]i) in the whole cell
configuration or with unaltered
[Cl]i using the
gramicidin-perforated patch approach. Prolonged GABA exposures elicited
reproducible decaying currents. The decay of IGABA
was associated with both a transient fall of conductance (gGABA) and shift of current reversal potential
(EGABA). The shift of EGABA
appeared to be time and driving force dependent. In the gramicidin-perforated patch configuration, repeated GABA exposures induced currents that gradually vanished. The fading of
IGABA was due to persistent shifts of
EGABA as a result of gGABA
recovering from one GABA application to another. In cells
alternatively clamped at potentials closely flanking resting potential
and submitted to a train of brief GABA pulses, a reversal of
IGABA was observed after 150 s recording. It is
demonstrated that, in intact frog melanotrophs, shifts of
EGABA combine with genuine receptor desensitization to depress IGABA. These findings strongly suggest
that shifts of EGABA may act as a negative
feedback, reducing the bioelectrical and secretory responses induced by
an intense release of GABA in vivo.
desensitization; intracellular chloride concentration; gramicidin-perforated patch recording
