Short applications of gamma-aminobutyric acid increase intracellular calcium concentrations in single identified rat lactotrophs

Anne Lorsignol, Anne Taupignon, Bernard Dufy
Neuroendocrinology. 1994-01-01; 60(4): 389-399
DOI: 10.1159/000126773

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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.

Author information:
(1)Laboratoire de Neurophysiologie, CNRS URA 1200, Université de Bordeaux II,
France.

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.

DOI: 10.1159/000126773
PMID: 7824081 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus