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Mammotropes and somatotropes in the adenohypophysis of androgenized female miceMorphological and immunohistochemical studies by light microscopy correlated with routine electron microscopy.

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THE ANATOMICAL RECORD 233:103-110 (1992)
Mammotropes and Somatotropes in the Adenohypophysis of
Androgenized Female Mice: Morphological and
lmmunohistochemical Studies by Light Microscopy Correlated With
Routine Electron Microscopy
AKIKO YAMAJI, FUMIHIKO SASAKI, YOSHIE IWAMA,
AND
SHOJI YAMAUCHI
Department of Veterinary Anatomy, University of Osaka Prefecture College of Agriculture,
Sakai, Osaka, Japan (A.Y.,F.S., S.Y.); and Department of Anatomy, Aichi Medical
University, Aichi, Japan (Y.I.)
ABSTRACT
Female mice were divided into androgenized (AF) and control
(CF) groups. The AF mice were injected subcutaneously with testosterone propionate (Tp) and the CF mice with sesame oil a t 5 days of age. Mammotropes (PRL
cells) and somatotropes (GH cells) in the adenohypophyses of these mice when they
became adults were studied with immunohistochemistry and morphometry by
light microscopy correlated with routine electron microscopy. In CF mice, almost
all of the PRL-immunoreactive cells (about 43% of all parenchymal cells) were type
I (classical) PRL cells, and almost all of the GH-immunoreactive cells (about 30%
of all parenchymal cells) were type I (classical) GH cells. Type I1 PRL cells accounted for about 0.4% of parenchymal cells, and type I1 GH cells were about 2.5%
of all parenchymal cells. In AF mice, the percentages of PRL and GH cells were not
significantly different from those of CF mice. Mammosomatotropes (Ms cells) in
both groups were less than 1%of all parenchymal cells. Numbers of all parenchymal, PRL and GH cells, however, were increased significantly in AF mice when
compared to those in CF, because the adenohypophysis was increased in volume in
AF mice. Type I PRL cells were larger in AF than in CF. The ultrastructure
suggested that type I PRL cells may show increased PRL synthesis and secretion
in AF mice. Furthermore, AF mice, in which the hypothalamus is masculinized by
the neonatal treatment with Tp, retained feminine characteristics in the population and size of PRL cells and GH cells in the adenohypophysis.
0 1992 Wiley-Liss, Inc.
There is a clear sex difference in adult mouse and rat
hypothalamus due to the absence or presence of testosterone during the neonatal period: the hypothalamus in female and male types controls the cyclic and
tonic secretion, respectively, of gonadotropins (Gn)
from the anterior pituitary gland (Pfeiffer, 1936; Harris, 1964; Barraclough, 1967; Gorski, 1968; Yazaki,
1968; MacLusky and Naftolin, 1981). Barraclough and
Leathem (1954) reported that the administration of
testosterone propionate (Tp) to neonatal female mice
causes the hypothalamus to become the male type and
results in infertility characterized by polycystic ovaries
that have numerous follicles of various sizes but no
corpora lutea. In such androgenized animals, prolactin
(PRL) levels in serum (Mallampati and Johnson, 1973,
1974; Cheng and Johnson, 1973174;Harlan and Gorski,
1977; Nakamura et al., 1988) and pituitary (Mallampati and Johnson, 1974) were reported to be increased
significantly when compared with those of controls.
However, no morphological evidence on the adenohypophysis in androgenized animals has been presented,
to our knowledge. This study was undertaken to get
new information on the influence of androgen on pituitary morphology in immature female mice, using immunohistochemistry by light microscopy correlated
0 1992 WILEY-LISS, INC.
with routine electron microscopy in a stereological
morphometric study.
MATERIALS AND METHODS
Animals
Primiparous mice of the SMA strain, bred in our animal quarters, were housed in cages under controlled
conditions with a constant temperature (24"C), 14 h r
light, 10 h r dark cycle, with food and water ad libitum.
To maintain uniform body growth, all of the litters
were reduced to 6 pups on the day of parturition and
weaned on day 25. Ten female pups were injected subcutaneously with Tp (1.00 mg) a t 5 days of age a s described by Barraclough and Leathem (1954). Ten female control mice received only injections of sesame
oil. All animals were killed a t 3 months of age.
Light Microscopic Study
To observe the development of ovarian follicles and
corpora lutea, ovaries of all mice were fixed for 22-24
Received February 11, 1991; accepted Setpember 25, 1991.
Address reprint requests to Dr. F. Sasaki, Department of Veterinary Anatomy, University of Osaka Prefecture College of Agriculture, Mozuume-machi, Sakai, Osaka 591, Japan.
104
A. YAMAJI ET AL
TABLE 1. Percentages (means f S.D.) of PRL cells and GH cells in the adenohypophysis of control and
androgenized mice’
Group of
mice (No.)
Control (5)
I
Androgenized (5)
Types of PRL cells (%)
I1
I
43.3 2 7.7
40.0 2 4.4
0.4 t 0.3
0.3 0.1
*
Types of GH cells (%)
+ I1
43.8
40.3
* 3.4
* 2.0
I
TI
30.5 2 3.9
27.8 2 4.1
2.5 2 1.1
5.2 2 3.6
T
+
TT
33.1 t 3.6
33.0 t 5.4
Ms cells
(%)
0-0.4
0.2-1.0
~
‘All data between two groups were analyzed by Student’s t test and Mann-Whitney’s U test.
TABLE 2. Numbers ( x
Group of
mice (No.)
Control (5)
Androgenized (5)
**P< 0.001.
lo4) of PRL cells and GH cells (means f S.D.) in the adenohypophysis of control and
androgenized female mice
Types of PRL cells ( x lo4)
I1
I + I1
Parenchymal
cells ( x lo4)
I
41.3 4.5
78.4 2 9.9**
17.9 2 4.1
30.6 2 6.0*
*
0.1 t 0.1
0.3 2 0.1*
18.1 i- 4.0
31.0 5 6.0*
Types of GH cells ( x
r
*
12.5 1.9
21.9 t 4.4*
TT
1.0 t 0.4
4.0 t 2.8
~~~
lo4)
T + IT
~
13.6 t 1.8
25.9 i- 5.0**
*P < 0.01 when compared with control female mice by Student’s t test.
h r in Bouin’s fluid, dehydrated in a graded series of
alcohols, and embedded in paraffin wax. Serial sections
(10 pm) were cut and stained with hematoxylin and
eosin.
To estimate the volume of the anterior pituitary
gland, the glands were obtained from 5 control (CF)
and 5 androgenized animals. After fixation in Bouin’s
fluid for 10 min in situ, the glands were carefully excised from the base of the skull. Then they were fixed
for 24 h r in the same fixative, dehydrated in a graded
series of alcohols, and embedded in paraffin wax. Serial
sections (10 pm in thickness) were cut and stained with
hematoxylin and eosin. Areas of the anterior pituitary
gland (Al, A,, . . ., A,) were measured with a Profile
projector (V-10, Nikon, Tokyo, Japan) and a Photopattern analyzer (PC-8001, Nippon Electric, Tokyo,
Japan). The volume (V) of the anterior pituitary gland
(pm3) was expressed as V = 10 x
A pm3, as described in a previous study (Sasaki and Sano, 1982).
The specificity of the immunohistochemical staining
was tested as follows. Normal rabbit serum was substituted for specific antiserum, and PRL and growth
hormone (GH) antisera were preabsorbed for 1day by
25 pg/ml mouse PRL provided by Dr. K. Komoto (University of Tokyo) and 25-50 pg/ml rat GH (UCB Bioproducts, Belgium), respectively.
xi
Electron Microscopic Study
The anterior pituitary glands from 10 mice (5 from
each group) were used for electron microscopy. To obtain electron micrographs evenly from all parts of the
anterior pituitary gland, a stereological morphometric
method described previously was used (Sasaki, 1974).
All pituitary glands were carefully excised from the
base of the skull and cut in the midsagittal plane. The
hemipituitary gland was discarded. To get good cytoplasmic preservation, the other half was diced into 6
small pieces, a s described previously (Sasaki, 1974).
All of the blocks were singly fixed in OsO, for 1 h r a t
4°C. This fixation method gives better exocytotic figures than one in which glutaraldehyde was first used.
The blocks wre dehydrated in a graded series of ethanol
solutions and embedded in Epon for 1 day at 60°C.
About 50 electron micrographs from each animal were
obtained. Parenchymal cells exhibiting a nucleus in
the micrograph totalled about 1,000 in each animal.
Two serial semithin sections adjoining each electron
micrograph were stained immunohistochemically by
antibodies to PRL or GH a s described previously
(Sasaki and Iwama, 1988). PRL-immunoreactive cells
were classified into type I PRL cells (classical type),
which contained irregularly shaped secretory granules,
and type I1 PRL cells, which contained small (100-200
nm in diameter), round secretory granules. GH-immunoreactive cells included type I GH cells (classical type)
which contained large (about 350 nm in diameter)
round secretory granules, and type I1 GH cells containing small (about 100-200 nm in diameter) round secretory granules. Mammosomatotropes (Ms cells) were
identified as those immunoreactive with both anti-PRL
and anti-GH; they contained small (about 100-200 nm)
round secretory granules, a s described previously
(Sasaki and Iwama, 1988).
Morphometry
Cell counts were made of parenchymal, PRL, GH,
and Ms cells on all electron micrographs described
above. All cells were identified by immunohistochemistry. The population of PRL and GH cells was expressed as a percentage and a number. The number of
parenchymal cells in each anterior pituitary gland was
calculated a s reported previously (Sasaki and Sano,
1982). A cellophane sheet describing a 15 cm unit
square (the value of 15 cm corresponds to 30 pm in an
Fig. 1. The anterior pituitary gland of a control female (CF) mouse.
A Type I PRL cells (nos. 3, 6-9, 12-15) contain irregularly shaped
secretory granules. Type I GH cells (nos. 2 , 5 , 11) contain large (about
350 nm in diameter) round secretory granules. Secretory granules in
exocytosis (arrow) are seen in a PRL cell. B: Stained with GH antiserum. C: Stained with PRL antiserum. D: A higher magnification of
the area indicated by the arrow in A. A, x 5,000; B,C, x 1,200; D,
x 20,000.
Fig. 1.
106
A. YAMAJI ET AL.
Fig. 2. The anterior pituitary gland in a n androgenized female (AF)
mouse. A: Type I PRL cells (nos. 2, 3) in AF contain generally more
abundant rough endoplasmic reticulum, Golgi apparatuses, and
secretory granules compared with those of CF mice. Secretory granules in exocytosis (arrows) in a PRL cell are seen. Type I GH cell (no.
1) in the AF mouse shows no morphological differences compared with
those in the CF mouse. B: Stained with GH antiserum. C: Stained
with PRL antiserum. D,E: Higher magnification views of the areas
indicated by the arrows in A. A, x 5,000; B,C, x 1,200;D,E, x 20,000.
electron micrograph of x 5,000) was superimposed onto
all electron microgrlaphs obtained. For each animal,
the mean number (N) of parenchymal cells with a nucleus in this square (900 em2) was counted and transformed into the number (N3”) of cells in the unit cube
(27,000 I J . ~ with
~ ) the sides of 900 pm2. The number of
parenchymal cells (T) was calculated by substituting
these values- into the formula of Sasaki and Sano
(1982): T = N3’2 x V/27,000. Numbers of GH and PRL
cells were calculated by multiplying T by the respective percentage of the types of cells obtained above.
To measure the sizes of type I PRL and GH cells, 50
cells of each type per animal showing a nucleus and
with the entire profile of the cell on the electron micrographs were chosen a t random. Each cellular area was
measured with a photopattern analyzer. The computer
automatically read the areas of individual cells. Areas
for each mouse were averaged, and the data reported
here are averages of data from 5 mice.
To compare the PRL synthetic function in PRL cells
between CF and AF animals, the areas of rough endoplasmic reticulum (RER) and of cytoplasm, except the
nucleus, in 30 cells/mouse pituitary were measured a t
the final magnification of x 10,000 by a point-counting
~
Fig. 3. The anterior pituitary gland in an androgenized mouse.
A.
Type I PRL cells (nos. 1-8) contain generally more rough endoplasmic
reticulum, Golgi apparatuses, and secretory granules compared with
those in the CF mouse. Secretory granules in exocytosis (arrows) occur more frequently than in the CF mouse. B-H: Higher magnification views of areas indicated by arrows in A. A, ~ 5 , 0 0 0 ;B-H,
x 20,000.
PRL AND GH CELLS IN ANDROGENIZED MICE
Fig. 3.
107
108
A. YAMAJI ET AL.
method, using a square lattice of points with a spacing
of 1 cm (in this case, the number of points corresponds
to the real number in pm2). RER is a good index for
expressing the PRL synthetic function morphologically
in PRL cells. The data were the averages of the data
from 5 mice. The data were expressed as the absolute
area (pm2)of RER or the relative area (%) of RER per
the area of the cytoplasm in a PRL cell.
Statistics
Student's t test and Mann-Whitney's U test were
used to compare the data from the two groups.
RESULTS
Light Microscopic Observation of Ovaries
Ovaries in CF mice contained many follicles and corpora lutea, while those in AF mice had numerous follicles of various sizes but no corpora lutea.
Morphometry
Body weight and volume of anterior pituitary gland
No difference in the body weight was found between
these two groups [CF: 25.5 2 2.2 g (mean t S.D.); AF:
25.1 t 2.0 gl. The volume of the anterior pituitary
gland, however, in AF mice [1.3 +- 0.2 mm3 (mean
S.D.)] was significantly larger (P < 0.01) than that of
CF mice (0.8 c 0.1 mm3).
*
PRL, GH, and Ms cells
Table 1 shows the percentages of PRL, GH, and Ms
cells. In CF mice, almost all of the PRL-immunoreactive cells (about 43% of all parenchymal cells) were
type I. Almost all of the GH-immunoreactive cells
(about 30%of all parenchymal cells) were type I. Only
a few type I1 PRL cells (about 0.4%) and type I1 GH
cells (about 2.5%) were found. No differences in percentage were found when PRL and GH cells in AF mice
were compared with those in CF. Ms cells were fewer
than 1% of all parenchymal cells in both groups of
mice.
The numbers of parenchymal, PRL, and GH cells are
presented in Table 2. In AF mice, the numbers of parenchymal (P < 0.001), of PRL (P < 0.011, and of GH
cells ( P < 0.001) were markedly increased when compared with those in CF mice.
The type I PRL cells were larger (P < 0.01) in AF
mice (107.7 t 2.0 pm2) than in CF mice (99.5 ? 2.4
pm2). There was no difference in the size of type I GH
cells between AF (118.8 t 9.5 pm2) and CF mice (124.9
10.1 pm2).
Type I PRL cells in AF mice also contained larger (P
< 0.01) areas of RER than those in CF mice: 27.4 5 2.9
pm2 vs. 17.8 ? 3.6 pm2 in absolute area, and 38.0 t
4.6% vs. 27.2 2 3.0% in the percentage of RER in the
cytoplasm of a PRL cell.
*
Ultrastructural Changes
In AF mice (Figs. 2, 3), type I PRL cells contained
more abundant secretory granules and rough endoplasmic reticulum and a better-developed Golgi complex
than those in CF mice (Fig. 1).The type I PRL cells also
included more secretory granules in exocytosis in AF
mice (Figs. 2,3) than those in a CF mouse (Fig. 1).Type
I GH cells in both AF and CF mice contained a number
of large (about 350 n m in diameter) and round granules. Although some difference was observed in the
content of small (100-200 nm in diameter) round secretory granules and of cell organelles among individual
cells for each group, no clear morphological differences
were found in type I1 PRL cells, type I and I1 GH cells,
or Ms cells between AF and CF mice.
DISCUSSION
This morphological study showed that synthesis and
secretion in PRL cells of the adenohypophyses in androgenized female mice increased significantly compared with that in controls. Thus, PRL cells in AF increased in number and size, in the frequency of
secretory granules in exocytosis, and in the development of cell organelles as compared with those in CF.
Radioimmunoassay data also has demonstrated that
PRL synthesis and secretion in the adenohypophysis
are greater in AF than in CF mice (Mallampati and
Johnson, 1973, 1974; Cheng and Johnson, 1973174;
Harlan and Gorski, 1977; Nakamura et al., 1988).
In this study, the numbers of GH a s well as PRL cells
in AF mice increased significantly over control levels.
Within spontaneous pituitary tumors in aging female
mice, the predominant cell types were PRL and GH
cells (Schechter et al., 1981). Thus, the adenohypophysis in AF resembled that of this pituitary tumor in the
increase in the number of PRL and GH cells.
It has been shown that the anterior pituitary gland
differentiates into the female type or male type due to
the absence or presence of a testis (or testosterone) during the neonatal period and then due to the presence or
absence of a n ovary (or estrogen andlor progesterone)
after puberty. A clear sex difference is observed in the
population and size of PRL cells and GH cells in the
anterior pituitary gland of adult mice; PRL cells are
more abundant and larger in female mice than in
males, and GH cells are more numerous in males
(Sasaki and Sano, 1980, 1982, 1983). By these criteria,
the anterior pituitary gland in AF mice is of the female
type.
It has been well documented that the sex differentiation in the release of gonadotropin-releasing hormones (GnRH) in the hypothalamus occurs during that
neonatal period named the critical period, due to the
presence or absence of a testis or testosterone (Harris,
1964; Barraclough, 1967; Gorski, 1968; MacLusky and
Naftolin, 1981). In fact, serum levels of testosterone in
male r a t pups during this period were significantly
higher than those in female pups (Pang et al., 1979;
Slob et al., 1980; Pang and Tang, 1984). In control female mice, since the hypothalamus becomes the female
type, it secretes GnRH cyclically after puberty; then,
the adenohypophysis can cyclically secrete gonadotropins (Gn). Thus, the female ovaries cyclically produce
follicles and corpora lutea (Gorski, 1968). The estrogen
and progesterone secreted cyclically from these ovaries
may lead their anterior pituitaries to the condition of
the normal female type by stimulating the glands.
On the other hand, in AF mice, the administration of
testosterone during the critical period leads the hypothalamus to secrete GnRH tonically after puberty;
then, the adenohypophysis secretes Gn tonically. Thus,
the ovaries of these AF mice contain only follicles but
no corpora lutea (Gorski, 1968). Estrogen secreted con-
PRL AND GH CELLS IN ANDROGENIZED MICE
tinuously from these follicles may lead their adenohypophyses to develop a prolactinoma by stimulating
PRL cells in the adenohypophysis.
The presence or absence of neonatal testosterone also
causes a sexual difference within the hypothalamus
that may account for sexually specific PRL release (Demarest et al., 1981; Gunnet and Freeman, 1982). This
mechanism may be the same as the one mentioned
above.
It has been reported that the administration of estrogen induces hypertrophy of the pituitary gland
(Wolfe and Wright, 1938; Ratner et al., 1963; Ramiretz
and McCann, 1964; Gersten and Baker, 19701, hyperplasia (Hymer et al., 1961; Shimazaki et al., 1962; Gersten and Baker, 1970; Lloyd et al., 1973) and marked
development of the endoplasmic reticulum and Golgi
complex of PRL cells (Hymer et al., 1961; Shimazaki et
al., 1962; Pantie and GenbaEev, 1969; Watari and
Tsukagoshi, 1969; Zambrano and Deis, 1970; Stratmann et al., 1974; Coates et al., 1975; Shiino and Rennels, 1976), and hyperactive secretion reflected by an
increased blood level of PRL (Ramiretz and McCann,
1964; Shinha et al., 1972; Yamamoto et al., 1975; Gudelsky et al., 1981). On the other hand, progesterone
partially inhibits the production (Haug and Gautvik,
1976) and secretion of PRL (Chen and Meites, 1970;
Caligaris et al., 1974). Since estrogen and progesterone
are secreted alternatively from ovaries in control adult
females, progesterone may inhibit their pituitary
glands to cause a prolactinoma. In AF mice, PRL cells
may originally increase in size and number due to the
stimulation of estrogen persistently secreted from polycystic ovaries. GH cells might secondarily increase in
number to maintain the anterior pituitary glands as
the female type in the percentage of PRL and GH cells,
as shown in this study.
ACKNOWLEDGMENTS
The authors thank Dr. K. Kohmoto (University of
Tokyo) for providing mouse PRL antiserum and mouse
PRL, and Dr. H. Seo (Nagoya University) for providing
GH antiserum.
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somatotrophs, adenohypophysis, light, electro, androgenized, micemorphological, immunohistochemical, correlates, microscopy, female, mammotropes, studies, routing
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