Publication: lmmunohistochemical localization of prolactin in functioning and regressing corpus luteum of pituitary autotransplanted rats
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Date
1986
Authors
Martín de las Mulas, J. ; Aguilar, E. ; Sánchez-Criado, J.E.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
In an attempt to shed light on the intimate
mechanism by which prolactin (PRL) switches from
supporting corpus luteum (CL) progesterone secretion (P)
to promote structural regression of the CL, day 2
(metestrous) autopituitary transplanted (APTr) rats were
used. In APTr rats the CL is under the only control of
PRL since an almost complete absence of LH and FSH
exist. The experimental group was given bromocriptine
(CB-154: 0.4 mg/day) on days 12, 13 and 14 of the cycle
and 0.25 ml of ethanol from day 15 to day 21. The control
group was given CB-154 from day 12 to day 21. Rats were
hemiovariectomized on day 12 to assess the morphological
characteristics of the active CL. PRL and P were
determined by RIA on days 12, 15 and 22. On day 12,
both PRL and P levels were higher than 80ng/ml
(luteotrophic action of PRL). On day 15, due to treatment
with CB- 154, the levels of both hormones had fallen below
7 ng/ml (functional luteolysis). On day 22, PRL levels were
again high ( > 50 ng/ml) in the shortly CB-154-treated rats
and low ( < 5 ng/ml) in the controls; the P levels were
lower than 5 ng/ml in both groups.
PRL-induced structural luteolysis in the experimental
group (hyperprolactinemic) was assessed by the structural
characteristics and by the CL weight loss on day 22 in
comparison with that exhibited by control rats. The
immunohistochemical staining of both endogenous and
total PRL in the lutein cells showed that the internalization
of PRL is not modified by the functional state of
the CL, nevertheless the intracellular redistribution of the
internalized hormone varied in relation with the PRL action
on the CL (luteotrophic, day 12vs luteolytic, day 22).These results seem to indicate that intracellular
mechanisms rather than receptor content determine CL
response to PRL.
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