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Department of Human Anatomy and Genetics, University of Oxford, Oxford, United Kingdom OX1 3QX
Address all correspondence and requests for reprints to: Prof. John F. Morris, Department of Human Anatomy and Genetics, University of Oxford, South Parks Road, Oxford, United Kingdom OX1 3QX. E-mail: john.morris{at}anat.ox.ac.uk
Rapid, nongenomic effects of testosterone on PRL release in
vitro were investigated. Anterior pituitary tissue from adult
male rats was stimulated in vitro for 5 or 20 min with
testosterone (T; 1 or 100 nM) or testosterone-BSA (T-BSA; 1
or 100 nM) with or without 1.2 mM tannic acid,
which enables visualization of secretory granule exocytosis. Within 5
min, both concentrations of T and T-BSA stimulated exocytosis from type
2 lactotrophs (characterized by small spherical granules), but not from
type 1 lactotrophs (characterized by large polymorphic granules). The
effects of T on type 2 lactotrophs could be blocked by preincubation
with dopamine (500 nM), but were not time or concentration
dependent, and could not be inhibited by 1) removal of extracellular
Ca2+, 2) the L-type Ca2+ channel blocker
nifedipine (100 nM), 3) the Ca2+-adenosine
triphosphatase inhibitor thapsigargin (150 nM), 4) the PKC
inhibitor retinal (10 µM), or 5) the
-aminobutyric
acidA chloride channel blocker picrotoxin (100
µM). T-BSA (0.1 nM to 1 µM)
for 5 or 20 min also caused an increased release of immunoreactive PRL
into the medium compared with control incubations. T and T-BSA did not
stimulate exocytosis from gonadotrophs or cause LH release. In
conclusion, we report for the first time a rapid, nongenomic effect of
T on PRL secretion.
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