Oestradiol 17β modifies fowl pituitary prolactin and growth hormone secretion in vitro

GENERAL

AND

COMPARATIVE

Oestradiol

ENDOCRINOLOGY

56, 299-307 (1984)

17p Modifies Fowl Pituitary Prolactin Hormone Secretion in Vitro

and Growth

T. R. HALL, S. HARVEY,* AND A. CHADWICK Department of Pure and Applied Zoology, The University of Leeds, Leeds, LS2 9JT, and * Wolfson Institute, The University of Hull, Hull, HU6 7RX, United Kingdom Accepted January 31, 1984 Chicken pituitary glands were incubated in medium containing oestradiol 17f3(E,), alone or together with single whole hypothalami. E, stimulated prolactin release from the pituitary and increased the prolactin releasing activity of the hypothalamus, but did not affect growth hormone release. Preincubation of pituitaries with E, dramatically stimulated subsequent prolactin release. Pituitaries primed with E, were more responsive to the prolactin-stimulating effects of hypothalamic extract (HE) and thyrotrophin-releasing hormone (TRH) and more sensitive to the prolactin-inhibiting effect of dopamine. E,-primed pituitaries were much less sensitive to the growth hormone releasing activity of TRH and HE. These results show that E2 may regulate pituitary function by direct effects on hormone release by modifying pituitary sensitivity to stimulatory or inhibitory influences and by altering hypothalamic

releasing

aCtiVity.

0 1984 Academic

Press, Inc.

The control of prolactin secretion in birds (Hall and Chadwick, 1979; Harvey et al., 1982; Chadwick and Hall, 1983; Hall, 1984) differs from that in mammals (Meites, 1972; Meites and Clemens 1972) in that the primary stimulus from the hypothalamus is stimulatory, whereas in mammals it is inhibitory. Stimulatory and inhibitory hypothalamic factors also control the release of growth hormone, with the stimulatory influence predominating in avian and mammalian hypothalamic extracts (Hall and Chadwick 1976, 1979; Harvey et al., 1979; Harvey, 1983). These prolactin and growth hormone releasing factors (Hall and Chadwick, 1983) have yet to be isolated from the avian hypothalamus, although the presence of thyrotrophin-releasing hormone (TRH), which stimulates both prolactin and growth hormone secretion (Hall et al., 1975; Harvey et al., 1978) has been demonstrated (Jackson, 1979). Inhibitory and stimulatory (Harvey et al., 1982; Harvey, 1983) biogenie amines have also been found in the avian hypothalamus (El Halawani and Burke, 1976; Jurani et al., 1978, 1981; El Halawani et al., 1980).

The control of prolactin and growth hormone secretion in birds is affected by various physiological states (e.g., dehydration), exogenous neurotransmitters (e.g., serotonin), and hormones (e.g., testosterone), (Hall, 1982; Harvey et al., 1982; Hall and Chadwick, 1982; Hall et al., 1984; Harvey et al., 1984). These agents may change prolactin and growth hormone release by direct pituitary action, by modifying the release of hypothalamic releasing factors, or by altering pituitary sensitivity to hypothalamic stimulation. Since oestradiol 17B (E2) is known to cause in vivo pituitary prolactin depletion (Kono et al., 1980) and stimulate prolactin release from pituitary-hypothalami coincubations (Hall and Chadwick, 1978), the possibility that E, may affect hypothalamic releasing activity or pituitary sensitivity to hypothalamic releasing factors has therefore been examined in the present study. In addition, since gonadal steroid pretreatment sensitises the somatotrophs of the mammalian pituitary to provocative stimuli (Malacara and Reichlin, 1972; Szabo and Frohman, 1975), the influence of oestradiol on in vitro

299 0016-6480184 $1.50 Copyright 0 1984 by Academic Press, Inc. AH rights of reproduction in any form reserved.

300

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AND CHADWICK

growth hormone secretion has also been determined in the domestic fowl. MATERIALS

and diluted with medium containing 0.01% ascorbic acid just before use. Clomiphene citrate (Sigma) which has antagonistic effects at pituitary and hypothalamic receptors for oestrogen and progesterone (Bowman et al., 1981; Terakawa et al., 1981) was dissolved in propyleneglycol:ethanol(7: 1 vol:vol) and diluted with medium before use. Control incubations also contained appropriate concentrations of the vehicles used. Hormone assays and statisticaf analyses. Prolactin concentrations in the media were determined by homologous radioimmunoassay (Scanes et al.. 1976; Lea et al., 1982). This assay has an intraassay variability of 2.5% and a minimum detection limit of 2.6 rig/ml. Growth hormone concentrations in some of the media were determined by the homologous radioimmunoassay of Harvey and Scanes (1977). The assay has an intraassay coefficient of variation of 4.1% and a minimal detectable dose of 0.75 &ml. Significant differences in the results were evaluated by Student’s ttest and by analysis of variance, with a level of significance of P < 0.05.

AND METHODS

Incubation technique. Adenohypophyses and hypothalami were dissected from the heads of freshly killed broiler fowl and placed in ice-cold medium 199 (Wellcome Reagents Ltd., Beckenham, England). Some of the pituitaries were treated with collagenase and pituitary cells prepared according to Bicknell and Follett (1975). Incubations were carried out for 2 hr in disposable tubes with 0.5 pituitary equivalents in 0.5 ml medium plus 0.5 ml medium containing the test substances. Following incubation the cells were separated by centrifugation and the media were appropriately diluted and stored deep frozen. The remaining pituitaries were bisected and each hemipituitary incubated separately, in 100 pl medium, according to the procedure described previously (Hall et al., 1975; Hall and Chadwick, 1978, 1983). The hemipituitaries were incubated for 3 hr although in some cases this occurred after a 20 hr preincubation period. The incubation media were aspirated following incubation and stored at - 20 Treatments. Some hemipituitaries were coincubated with a whole mediobasal hypothalamus as described previously (Hall, 1982; Hall and Chadwick, 1983). The remaining hypothalami were extracted in 0.1 N HCI (Hall et al., 1975) and this extract (HE) was added to some pituitary cell or hemipituitary incubations. A stock solution of oestradiol 17p was made in 95% ethanol and appropriately diluted with medium 199 for in vitro incubations. Control incubations contained equivalent amounts of ethanol. Synthetic thyrotrophin-releasing hormone (TRH) (Reckitt and Colman, Hull, England), was dissolved in distilled water and diluted with medium just before use. Dopamine HCl (Sigma, Poole, England) was dissolved in 0.001 N HCl

EFFECTS OF OESTRADIOL

RESULTS

The release of prolactin from dispersed pituitary cells was increased, to a similar extent, by 3.7 x 10P5and 3.7 x 10v7M E, (Table 1). HE also stimulated the release of prolactin (P < O.OOl), but this stimulation was not enhanced by the presence of E, in the incubation media (Table 1). Growth hormone release was significantly increased by HE incubation, although in the presence of 3.7 x 10e5 A4 E, the magnitude of this stimulation was greatly (P < 0.01) reduced (Table I). E, had no effect on basal growth hormone release.

TABLE 1 17p ON RELEASE OF PROLACTIN AND GROWTH HORMONE PITUITARY

Treatment Medium 199 (control) HE Oestradiol 17B (3.7 x lo-’ M) Oestradiol + HE Oestradiol 17p (3.7 x 10m5 M) Oestradiol + HE Note. A cell suspension equivalent equivalent to 0.5 hypothalamus for 2 * P < 0.05, significantly diierent ** P < 0.05, significantly different

FROM DISPERSED

FOWL

CELLS IN VITRO

Prolactin (ng * ml-‘) 245 1402 340 1240 369 1368

‘2 + -t ” 2

16 (27) 56 (17)* 18 (25)** 24 (14)* 22 (26)** 45 (13)*

Growth hormone (ng . ml-‘) 340 930 290 830 320 640

k 40 (25) rf: 60 (12)* k 40 (25) ” 60 (12)* 2 30 (24) -+ 50 (12)*,**

to 0.5 pituitary was incubated alone or with hypothalamic extract (HE) hr. Results show means f SE (N). from treatment without HE. from control.

E2 EFFECTS

ON PROLACTIN

301

AND GH

The release of prolactin (P < 0.001) and growth hormone (P < 0.05) from incubated hemipituitary glands was similarly increased by HE treatment (Table 2). E2 again stimulated basal prolactin release but had no effect on HE-induced prolactin secretion or on basal growth hormone release. The highest dose of E, again reduced (P < 0.05) HE-stimulated growth hormone secretion (Table 2). The stimulation of prolactin release by E, was, however, blocked when clomiphene (an antioestrogen) was added to the incubation media (Table 2). When incubated with lower doses, the prolactin response to E, was dose related (Table 3). Prolactin release was also increased in the presence of whole hypothalamic tissue and its prolactin-releasing activity was further increased, in a dose-related way, by addition of E, (Table 3). The stimulatory dose-related effect of E, on basal prolactin release was also observed 20 hr after E, incubation (Table 4); the magnitude of the response also being enhanced in comparison with short-term incubation (Table 3). In a subsequent experiment the possibility that E, pretreatment may effect pituitary responsiveness was examined. As expected E, priming significantly (P < 0.01) increased the basal release of prolactin

TABLE EFFECTS PROLACTIN INCUBATED MEDIOBASAL

3

OF OESTRADIOL 17p ON RELEASE OF FROM FOWL HEMIPITUITARY GLANDS ALONE (AP ONLY) OR COINCUBATED HYPOTHALAMIC TISSUE (AP + FOR 3 hr Prolactin (ng . fng-I

Tkeatment Medium Oestradiol

199 (control) 17p-10-‘0 M 10-g M IOmR M IO-‘M

AP only 43.0 48.4 55.2 55.8 80.0

-t 1.8 2 1.9 c 4.6 -+ 1.6* t 10.9*

WITH HYPO)

release pituitary) AP + HYPO 71.1 80.7 105.3 124.5 158.9

NOM. Results show mean 5 SE (N = 5). * P < 0.05, significantly different from control.

2 5.4 k 2.9 2 9.0 + 4.2* 2 24.5*

302

HALL,

HARVEY,

AND CHADWICK

TABLE 4 EFFECTS OFPREINCUBATION WITH OESTRADIOL 17po~ SUBSEQUENTRELEASE OFPROLACTIN FROM FOWL HEMIPITUITARY GLANDS IN VITRO

0.5 and 1.0 hypothalamic equivalents (Fig. 1). Incubation with TRH had a biphasic effect on prolactin release (Fig. 2). Although Prolactin release each dose of TRH stimulated (P < 0.05) Pretreatment (ng * mg-’ pituitary) prolactin secretion, the response to the highest dose (lop6 M) was less (P < 0.05) Medium 199 (control) 32.3 5 3.2 Oestradiol 17B-lo-to M 60.4 k 8.8* than that to a lower dose (1O-7 M). Pre105.2 t 11.1* 1O-9 M treatment with E, again increased basal 141.6 ? 10.9* 1O-8 M prolactin release and augmented (P < 0.05) lo-’ M 140.7 * 20.0* the stimulatory effect of TRH, the prolactin Note. Hemipituitaries were preincubated for 20 hr response to each dose being more than adin medium or in medium containing oestradiol 17B, ditive. Growth hormone release was enfollowing which they were incubated in medium 199 hanced (P < 0.05) by 10e7 and 10e6 M for 3 hr. Results show means ? SE (N = 5). TRH, although E, pretreatment blocked * P < 0.05, significantly different from control. this response (Fig. 2). The potentiation of the prolactin re(Fig. 1). Incubation with HE induced a sig- sponse of E,-primed pituitaries to TRH was ificant (P < 0.001) dose-related increase in also dose related (Fig. 3a) as was the basal prolactin release (Fig. 1). For each dose, level of prolactin release. In each case the the magnitude of the prolactin increase was maximum prolactin response (Fig. 3b) occurred with 10e8 M TRH. enhanced (P < 0.01) by E, pretreatment, The stimulation of prolactin release by the responses to 0.5 and 1.0 hypothalamic equivalents being more than additive (Fig. lo-'M TRH was reduced (P < 0.05) when lop7 M or lop6 M dopamine was also 1). Although E, had no effect on basal present (Fig. 4). Pretreatment with E, again growth hormone release, it completely reblocked the stimulatory (P < 0.05) effect of increased (P < 0.001) the prolactin 800-

4 1

800-

o]od’o.is Hypothalamic

0.5

1.0

Equivalents

FIG. 1. Release of prolactin and growth hormone from chicken hemipituitary glands incubated with different doses of chicken hypothalamic extract. The pituitary glands were preincubated for 20 hr in the presence (open symbols) or absence (solid symbols) of lo-‘M oestradiol 17B. Means +- SEM (N = 5 or 6).

E2 EFFECTS

0’

-I0

ON PROLACTIN

O10-g

10-a

10-7

10-S Dose

of TRH

AND GH

-IA 0

10-g

10-a

303

10-7

10-C

(MI

FIG. 2. Release of prolactin and growth hormone from chicken hemipituitary glands incubated with different doses of thyrotrophin-releasing hormone (TRH). The pituitary glands were preincubated for 20 hr in the presence (open symbols) or absence (solid symbols) of lo-’ M oestradiol 17p. Means + SEM (N = 6).

(b)

350

300

250

250 1

2 E G c 200

200-

.E 2 ;

G E 2 E 150a

150

li

100

.r i; _m loo0 p’

50

50 1

0

‘/A 0

OJ 10-S Dose

10-e of

TRH

(MI

10.’ Dose

of Oestradiol

178

(MI

FIG. 3. Release of prolactin from chicken hemipituitary glands (a) incubated with different doses of TRH following preincubation with lo-lo (0), 10v9 (A), 10e8 (m), or 10-‘(A) M oestradiol 17p or in medium 199 alone (0); (b) the increase in the release of prolactin with 1O-8 M TRH compared to incubation in medium alone following priming with different concentrations of oestradiol 17S. Means ?I SEM (N = 6).

304

HALL,

HARVEY,

AND CHADWICK

01F/A

0’ we-e 0

0

Dose

of Dopamine

(MI

with

10-b

10-9

10-a

10-7

10-Q

TRH

FIG. 4. Effects of TRH and dopamine on the release of prolactin and growth hormone from control (0) and oestradiol-primed (0) fowl pituitary glands. Hemipituitary glands were preincubated for 20 hr in medium alone or in medium containing IO-’ M oestradiol, before a 4-hr incubation in medium containing lo-’ M TRH in the presence of different doses of dopamine. Means 2 SEM (N = 6).

sponse to TRH and increased pituitary sensitivity to dopamine inhibition, low9 M dopamine significantly (P < 0.05) reducing the response to TRH (Fig. 4). Growth hormone release from control, but not E,-primed pituitaries was again stimulated (P < 0.05) by TRH. Dopamine had no significant effect on basal or stimulated growth hormone release. DISCUSSION

These results demonstrate that E, is a potent prolactin secretagogue in birds, as it is in mammalian species (Meites, 1972; Meites and Clemens 1972). These results confirm our preliminary in vitro data (Hall and Chadwick, 1978) and are in agreement with the observation of increased plasma prolactin levels in ovariectomised turkeys given oestradiol benzoate treatment (El Halawani et al., 1982). The E, stimulation of prolactin secretion was reversed by the antagonist clomiphene, suggesting it acts at specific oestrogenic receptors. The results reported here show a clear stimulatory effect of E, priming on basal prolactin release, an effect that continues

for at least several hours in the absence of the gonadal steroid in the incubation media (Table 4). Synthesis rates were not measured in these experiments, so it is not clear if the steroid affects only the release of prolactin or whether biosynthesis is also enhanced. E, may have a direct action on the release process, since it was effective in short-term (2-3 hr) incubations. However, a 20-hr exposure to the steroid was more effective in enhancing prolactin release, presumably because this allows sufficient time for any transcriptional or translational responses to develop. In mammals, the mechanism of El-stimulated prolactin secretion involves an induction of DNA synthesis and consequently an elevated production of preprolactin RNA (Lieberburg and McEwen, 1979). E, did not affect the response to HE when added concurrently in incubation (Tables 1 and 2), but enhanced hypothalamus-stimulated prolactin release (Table 3), suggesting that E, also stimulates hypothalamic prolactin releasing activity. Oestrogens may inhibit the release of hypothalamic prolactin inhibiting hormones in

E2 EFFECTS

ON

PROLACTIN

mammals (Meites 1972; Meites and Clemens, 1972). Avian HE possesses prolactin and growth hormone stimulating activities (Tixier-Vidal and Gourdji, 1972; Hall et al., 1975; Hall and Chadwick, 1979, 1983; Harvey et al., 1979, 1982), though the presumptive releasing hormones have only been partially separated (Hall and Chadwick, 1983). In the present study the stimulatory effect of HE on in vitro growth hormone release was reduced in the presence of E,. Preincubation of E, also dramatically altered subsequent prolactin and growth hormone responses to provocative stimuli. Prolactin secretion was considerably elevated, whereas growth hormone responses were completely abolished when HE was added to incubation media. In contrast with prolactin, E, did not affect basal release of growth hormone, either in incubations or following preincubation with the steroid. The inhibitory effect of E, on growth hormone secretion in the chicken contrasts with its stimulatory effect in mammalian species (Szabo and Frohman, 1975). The effects of TRH on pituitary function in birds are well documented. Following the observation that the peptide could stimulate TSH release in vitro (Scanes, 1974), we showed that it had in vitro prolactin and growth hormone releasing activity in the pigeon and the domestic fowl (Hall et al., 1975; Hall and Chadwick, 1976; Harvey et al., 1978). The in vivo responses to TRH may, however, depend upon the physiological condition of the birds (Harvey et al., 1981). Though Harvey et al. (1981) found no difference in the in vivo growth hormone response to TRH in intact and gonadectomized fowl, the present results show that the in vitro response is altered by E, treatment. As shown in Fig. 2 the growth hormone response was completely absent following E, pretreatment, whereas the prolactin response to TRH was enhanced following exposure of the pituitary glands to E,. Further examination of the prolactin

AND

GH

305

response (Fig. 4) showed that the enhancement of the response to TRH was dependent upon the pretreatment concentration of EZ. This change in responsivity to TRH is similar to the situation seen in the rat, where oestrogen pretreatment in vivo produces a sensitivity of the prolactin cells to TRH that is not present in control animals. This response is apparently due to an induction of TRH binding sites in the pituitary (de Lean et al., 1977). In addition Raymond et al. (1978) demonstrated that both basal and TRH-stimulated release of prolactin from rat pituitary cells in vitro were stimulated following a 120-hr preincubation with 1O-9 M E,. Dopamine may be a prolactin inhibiting factor in birds (Nistico et al., 1979, 1980; Hall, 1982, Harvey et al., 1982; Hall and Chadwick, 1983), as it is in mammals (Raymond et al., 1978; Weiner and Ganong, 1978). Dopamine has little effect on basal release of prolactin in vitro, but inhibits TRH and hypothalamus-stimulated release of the hormone (Hall, 1982). In the present experiments (Fig. 3) dopamine inhibited the TRH-stimulated release of prolactin from both the control and E,-primed pituitaries, in a concentration-related fashion. Dopamine not only reversed the stimulation of prolactin attributable to TRH, but at the highest concentration it also blocked the E2-induced rise in prolactin release. In addition, the E,-primed pituitaries appeared to be more sensitive to the inhibitory action of dopamine. The amine had no significant effect on the release of growth hormone from either control or E,-primed pituitary glands, confirming other reports on the lack of direct amine effects on avian pituitary somatotrophs (Hall, 1982; Harvey, 1983). The prolactin response to dopamine is similar to that seen in mammals, where the TRH-stimulated release of prolactin was inhibited in a concentration-related fashion by a dopamine agonist (Raymond et al., 1978).

In conclusion,

these results show that E,

306

HALL,

HARVEY,

has a direct action on the pituitary gland and on the hypothalamus to increase the release of prolactin, but does not affect growth hormone release by itself. The steroid increases prolactin cell sensitivity to the stimulatory actions of HE and TRH and to the inhibitory action of dopamine, whereas it decreases growth hormone ceII sensitivity to the stimulatory actions of HE and TRH. ACKNOWLEDGMENT This work was supported, in part, by grants from the Leeds Philosophical and Literary Society and by the Science Research Council (CR/B 47782).

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AND CHADWICK vertebrates-a comparative survey. Gen. Pharmacol. 15, 189-195. Hall, T. R., and Chadwick, A. (1976). Effects of growth hormone inhibiting factor (somatostatin) on the release of growth hormone and prolactin from pituitaries of the domestic fowl in vitro. J. Endocrinol. 68, 163-164. Hall, T. R., and Chadwick, A. (1978). Effects of oestradiol 17p and testosterone on prolactin secretion by the pituitary of the domestic fowl in vitro. IRCS Med. Sci. 6, 327. Hall, T. R., and Chadwick, A. (1979). Hypothalamic control of prolactin and growth hormone secretion in different vertebrate species. Gen. Coma. Endocrinol. 37, 333-342. Hall, T. R., and Chadwick, A. (1982). Serotonin mediation of osmotic stress-induced prolactin secretion in the fowl. J. Endocrinol. 94, 26 P. Hall, T. R., and Chadwick, A. (1983):Hypothalamic control of prolactin and growth hormone secretion in the pituitary gland of the pigeon and the chicken: in vitro studies. Gen. Comp. Endocrinol. 49, 135- 143. Hall, T. R., Chadwick, A., Bolton, N. J., and Scanes. C. G. (1975). Prolactin release in vitro and in vivo in the pigeon and the domestic fowl following administration of synthetic thyrotrophin-releasing factor (TRF). Gen. Camp. Endocrinol. 25, 298306. Hall, T. R., Harvey, S.. and Chadwick, A. (1984). Inhibition by testosterone of prolactin and growth hormone release from chicken anterior pituitary glands in vifro. J. Endocrinol. 102, 153-159. Harvey, S. (1983). Neuroendocrine control of growth hormone secretion in birds. In “Progress in Nonmammalian Brain Research” (G. Nistico and L. Bolis. eds.). Vol. 3 pp. 207-237. CRC Press, Boca Raton. Harvey, S., Chadwick, A., Border, G., Scanes, C. G., and Phillips, J. G. (1982). Neuroendocrine control of prolactin secretion. In “Aspects of Avian Endocrinology: Practical and Theoretical Implications” (C. G. Scanes, M. A. Ottinger. A. D. Kenny, J. Balthazart, J. Cronshaw, and 1. Chester-Jones, eds.). pp. 41-64. Grad. Studies, Texas Tech Univ., Lubbock. Harvey, S., Hall, T. R.. and Chadwick. A. (1984). Growth hormone and prolactin secretion in waterdeprived chickens. Gen. Comp. Endocrinol. 54, 46-50. Harvey, S., Scanes, C. G., Chadwick. A., and Bolton, N. J. (1978). The effect of thyrotrophin-releasing hormone (TRH) and somatostatin (GHRIH) on growth hormone and prolactin secretion in vitro and in vivo in the domestic fowl. (Callus domesticus). Neuroendocrinology 26, 249-260. Harvey, S., Scanes, C. G., Chadwick, A., Border, G.,

E2 EFFECTS

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Tixier-Vidal, A., and Gourdji, D. (1972). Cellular aspects of the control of prolactin secretion in birds. Gen. Comp. Endocrinol. Suppl. 3, 51-64. Weiner, R. I., and Ganong, W. E (1978). Role of brain monoamines and histamine in regulation of anterior pituitary secretion. Physiol Rev. 58, 905-976.