Short applications of gamma-aminobutyric acid increase intracellular calcium concentrations in single identified rat lactotrophs
Neuroendocrinology. 1994-01-01; 60(4): 389-399
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1. Neuroendocrinology. 1994 Oct;60(4):389-99.
Short applications of gamma-aminobutyric acid increase intracellular calcium
concentrations in single identified rat lactotrophs.
Lorsignol A(1), Taupignon A, Dufy B.
(1)Laboratoire de Neurophysiologie, CNRS URA 1200, Université de Bordeaux II,
We have investigated the direct effect of GABA receptor agonists on the cytosolic
free calcium concentration ([Ca2+]i) and the membrane potential of rat
lactotrophs in primary culture. [Ca2+]i was recorded in single identified
lactotrophs by dual emission microspectrofluorimetry using indo-1 as
intracellular fluorescent calcium probe. Whole cell and perforated patch-clamp
were performed. A short application of GABA (10(-5) M, 10 s) induced a marked
transient [Ca2+]i increase in 66% of lactotrophs, which could be readily mimicked
by muscimol (10(-5) M). By contrast, neither L-homocarnosine (10(-3) M) nor
baclofen (10(-5) M), a GABAB agonist, had any effect on [Ca2+]i. The GABA-induced
[Ca2+]i increase was antagonized by picrotoxin (10(-5) M), bicuculline methiodide
(10(-5) M) and strychnine (10(-4) M), demonstrating GABAA receptor specificity.
Furthermore, clonazepan (1.5 x 10(-4) M) could potentiate the GABA effect on
[Ca2+]i. The [Ca2+]i increase disappeared in the absence of Ca2+ in the
extracellular medium or in the presence of Ca2+ channel blockers (cadmium, PN
200-110). GABA and muscimol depolarized the membrane potential with a concomitant
fall in cell input resistance, thus suggesting, as in other cell types, the
opening of receptor-operated chloride channels. When Ca2+ entry was prevented by
the use of cadmium (500 x 10(-6) M), GABA still elicited membrane depolarization
but did not raise [Ca2+]i. Our results suggest that a short application of GABA
leads to Ca2+ entry through voltage-gated Ca2+ channels in single lactotrophs.
This Ca2+ influx is due to depolarization of the prolactin cell.
PMID: 7824081 [Indexed for MEDLINE]