THE COMBINED EFFECT OF MONOAMINE OXIDASE INHIBITORS AND CORTICOSTEROIDS ON THE PITUITARY-GONADAL SYSTEM OF MALE RATS

SUMMARY The mechanism by which combined treatment with monoamine oxidase inhibitors and a corticosteroid reduces the weight of the accessory sex glands in intact rats by about one half has been studied. Phenelzine sulphate in combination with hydrocortisone acetate given for 30 days to ovariectomized rats reduced the pituitary stores of luteinizing hormone (LH) by 33%. Similar reductions in somatotrophic hormone, corticotrophin and thyroid-stimulating hormone content were found after comparable treatment, whereas luteotrophic hormone increased. The increase of weight of the seminal vesicles and prostate gland produced by human chorionic gonadotrophin could be partly antagonized by the simultaneous administration of mebanazine and dexamethasone, but the action of testosterone on these glands in castrated animals was not inhibited. Interference with the production and effectiveness of LH is therefore the most likely mode of action by which these drugs effect the reduction of the weight of the accessory sex glands.

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POSSIBLE ROLE OF 5α-ANDROSTANE-3α,17β-DIOL IN THE CONTROL OF FOLLICLE-STIMULATING HORMONE SECRETION IN THE IMMATURE FEMALE RAT

Journal of Endocrinology ◽

10.1677/joe.0.0920037 ◽

1982 ◽

Vol 92 (1) ◽

pp. 37-42 ◽

Cited By ~ 10

Author(s):

H. M. A. MEIJS-ROELOFS ◽

P. KRAMER ◽

L. GRIBLING-HEGGE

Keyword(s):

Inhibitory Action ◽

Combined Treatment ◽

Hormone Secretion ◽

Inhibitory Effect ◽

Ovariectomized Rats ◽

Female Rat ◽

Immature Rat ◽

Rat Strain ◽

Intact Rats

A possible role of 5α-androstane-3α,17β-diol (3α-androstanediol) in the control of FSH secretion was studied at various ages in ovariectomized rats. In the rat strain used, vaginal opening, coincident with first ovulation, generally occurs between 37 and 42 days of age. If 3α-androstanediol alone was given as an ovarian substitute, an inhibitory effect on FSH release was evident with all three doses tested (50, 100, 300 μg/100 g body wt) between 13 and 30 days of age; at 33–35 days of age only the 300 μg dose caused some inhibition of FSH release. Results were more complex if 3α-androstanediol was given in combined treatment with oestradiol and progesterone. Given with progesterone, 3α-androstanediol showed a synergistic inhibitory action on FSH release between 20 and 30 days of age. However, when 3α-androstanediol was combined with oestradiol a clear decrease in effect, as compared to the effect of oestradiol alone, was found between 20 and 30 days of age. Also the effect of combined oestradiol and progesterone treatment was greater than the effect of combined treatment with oestradiol, progesterone and 3α-androstanediol. At all ages after day 20 none of the steroid combinations tested was capable of maintaining FSH levels in ovariectomized rats similar to those in intact rats. It is concluded that 3α-androstanediol might play a role in the control of FSH secretion in the immature rat, but after day 20 the potentially inhibitory action of 3α-androstanediol on FSH secretion is limited in the presence of oestradiol.

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Controlled trial of trimipramine, monoamine oxidase inhibitors, and combined treatment in depressed outpatients.

BMJ ◽

10.1136/bmj.2.6201.1315 ◽

1979 ◽

Vol 2 (6201) ◽

pp. 1315-1317 ◽

Cited By ~ 64

Author(s):

J P Young ◽

M H Lader ◽

W C Hughes

Keyword(s):

Monoamine Oxidase ◽

Controlled Trial ◽

Combined Treatment ◽

Monoamine Oxidase Inhibitors

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A FEMALE-LIKE RISE IN LUTEINIZING HORMONE AND FOLLICLE-STIMULATING HORMONE AFTER GONADECTOMY IN MALE RATS INDUCED BY OESTRADIOL PRETREATMENT

Journal of Endocrinology ◽

10.1677/joe.0.0800111 ◽

1979 ◽

Vol 80 (1) ◽

pp. 111-116 ◽

Cited By ~ 4

Author(s):

S. N. JUSTO ◽

A. NEGRO-VILAR

Keyword(s):

Sexual Difference ◽

Female Rats ◽

Male Rats ◽

Ovariectomized Rats ◽

Serum Concentrations ◽

Control Male ◽

Male And Female Rats ◽

Series Of Experiments ◽

And Control ◽

Intact Rats

A marked sexual difference in the rise of serum gonadotrophin concentrations after gonadectomy has been described in the rat. Gonadectomy in males induced a rapid rise in the concentrations of both LH and FSH within 8 to 12 h, whereas ovariectomy invoked a rapid increase in the concentration of FSH while the response by LH was delayed for several days. To determine whether these differences could be explained, at least in part, by the different steroid milieu at the time of gonadectomy, a series of experiments were performed to analyse the rise in both LH and FSH serum concentrations in control male and female rats and in male rats that had been pretreated with oestradiol-17β. Adult male rats received an s.c. implant of a silicone elastomer capsule filled with crystalline oestradiol-17 β. Controls received empty capsules. Twenty-four hours later, the oestradiol-implanted rats were castrated and control animals were sham-operated. Both LH and FSH levels remained within control levels after castration in the oestradiol-implanted rats, indicating that the oestradiol implant was preventing any rise of either gonadotrophin. On day 5 after implantation, the capsules were removed, sham-implanted animals were castrated and LH and FSH levels at 12, 24, 48 and 72 h were measured and compared with those of ovariectomized rats at similar intervals. The control male rats displayed the pattern of gonadotrophin increments normally found after castration, with both LH and FSH concentrations rising significantly by 12 h after castration and with further increments at later periods. Oestradiol-treated rats showed a female-like gonadotrophin pattern. FSH levels started to rise significantly at 24 h compared with values from intact rats and increased further at 48 and 72 h. During the first 48 h, FSH levels in both oestradiol-treated, castrated rats and female gonadectomized rats were significantly lower than in castrated animals. LH levels, on the other hand, remained low in both groups during the first 48 h, starting to rise significantly above control levels by 72 h. These results indicate that the different pattern of response to gonadectomy in rats of both sexes may be altered by changes in steroid environment and, therefore, may not be genetically predetermined.

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Effects of monoamine oxidase inhibitors on the copulatory behavior of male rats

Psychopharmacology ◽

10.1007/bf00403640 ◽

1972 ◽

Vol 24 (2) ◽

pp. 209-217 ◽

Cited By ~ 14

Author(s):

Donald A. Dewsbury ◽

Harry N. Davis ◽

Paul E. Jansen

Keyword(s):

Monoamine Oxidase ◽

Copulatory Behavior ◽

Monoamine Oxidase Inhibitors ◽

Male Rats

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REGULATION OF PROLACTIN BINDING SITES IN THE SEMINAL VESICLE, PROSTATE GLAND, TESTIS AND LIVER OF INTACT AND CASTRATED ADULT RATS: EFFECT OF ADMINISTRATION OF TESTOSTERONE, 2-BROMO-α-ERGOCRYPTINE AND FLUPHENAZINE

Journal of Endocrinology ◽

10.1677/joe.0.0810011 ◽

1979 ◽

Vol 81 (1) ◽

pp. 11-18 ◽

Cited By ~ 28

Author(s):

R. J. BARKEY ◽

J. SHANI ◽

D. BARZILAI

Keyword(s):

Seminal Vesicle ◽

Binding Sites ◽

Specific Binding ◽

Prostate Gland ◽

Male Rats ◽

Male Rat ◽

Serum Prolactin ◽

Testosterone Replacement Therapy ◽

Adult Rats ◽

Intact Rats

The effect of hormonal manipulations on prolactin binding to its specific binding sites in the seminal vesicle, prostate gland, testis and liver of adult male rats was studied. Castration significantly reduced prolactin binding to the seminal vesicle and prostate, whereas it greatly increased its binding to the liver. Testosterone replacement therapy restored the reduced level of binding to that found in the liver of intact rats, whereas binding to the seminal vesicle and the prostate was raised to the high levels found in the testosterone-treated intact rats. In contrast, testosterone administration to intact rats significantly reduced the binding of prolactin to the testicular homogenate. The administration of 2-bromo-α-ergocryptine (CB 154) to either intact or testosterone-treated castrated rats caused no significant change in binding of prolactin to any of the organs tested. Fluphenazine enanthate or CB 154 +ovine prolactin increased the binding of prolactin to the liver, when compared with untreated rats, whereas in the testis these treatments resulted in a minor decrease as compared with untreated rats. In the testosterone-treated castrated rats, fluphenazine caused no apparent effect on the binding of prolactin to any of the organs tested. In conclusion, testosterone is essential for the maintenance of prolactin binding sites in the seminal vesicle and prostate of the adult rat. Prolactin, however, does not appear to regulate its own receptor in the accessory sex glands, neither alone nor in synergism with testosterone. In the testis, exogenous testosterone exerted a negative effect on prolactin binding, as did raised serum prolactin levels. In the liver of the male rat, testosterone seemed to be the major cause of the low level of prolactin binding sites, while prolactin was capable of inducing its own sites in that organ.

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MECHANISM(S) BY WHICH ADRENALECTOMY AND CORTICOSTERONE INFLUENCE PROLACTIN RELEASE IN THE RAT

Journal of Endocrinology ◽

10.1677/joe.0.0870131 ◽

1980 ◽

Vol 87 (1) ◽

pp. 131-NP ◽

Cited By ~ 30

Author(s):

F. C. LEUNG ◽

H. T. CHEN ◽

S. J. VERKAIK ◽

R. W. STEGER ◽

J. J. PELUSO ◽

...

Keyword(s):

Serum Levels ◽

Thyroid Stimulating Hormone ◽

Significant Inhibition ◽

Male Rats ◽

Prolactin Release ◽

Medial Basal Hypothalamus ◽

Hypophysectomized Rats ◽

Adrenalectomized Rats ◽

Intact Rats

The possible direct effect of corticosterone on release of pituitary prolactin was examined in a system using incubation for 8 h. Corticosterone at either 0·1 or 1 μg/ml medium had no significant effect on in-vitro prolactin release but 10 or 100 μg/ml medium produced a significant inhibition of release of prolactin. Release of LH, FSH and thyroid-stimulating hormone were not altered by 0·1, 1 or 10 μg corticosterone/ml, indicating that its action at the concentration of 10 μg/ml was specific on release of prolactin. Corticosterone injected at doses of 1 or 5 mg/kg into hypophysectomized rats with two pituitary grafts underneath the kidney capsule produced a significant fall in serum levels of prolactin when compared with control hypophysectomized rats with two pituitary grafts. Examination with the electron microscope showed that about one third of the lactotrophes from adrenalectomized rats after corticosterone injection exhibited patterns which suggested a decrease in protein synthesis when compared with lactotrophes from adrenalectomized rats given only the vehicle injection. These observations indicated that inhibition of release of prolactin by corticosterone could be exerted directly on the pituitary gland, and that the rise of serum levels of prolactin after adrenalectomy might have been due to the removal of direct inhibition by corticosterone. Male rats were adrenalectomized and 2–3 weeks later, concentrations of dopamine and noradrenaline in the medial basal hypothalamus were measured and found not to be different from values in intact rats. Dopamine metabolism also was not altered in the median eminence. The dopaminergic agonist, l-DOPA, inhibited, and the antagonists, pimozide and haloperidol, stimulated release of prolactin in both adrenalectomized and intact rats. Serotonin (5-HT) metabolism in the medial basal hypothalamus and anterior hypothalamus of adrenalectomized rats was not significantly different from values in intact rats, but a higher concentration of 5-HT was observed in the medial basal hypothalamus of adrenalectomized rats when compared with the values in intact rats. A serotonergic agonist, fluoxetine, and an antagonist, cyproheptadine, had no apparent effect on release of prolactin in intact rats, but fluoxetine produced a significant rise, and cyproheptadine, a significant lowering of serum levels of prolactin in adrenalectomized rats. These results suggest that 5-HT, but not dopamine, may be involved in the rise of prolactin after adrenalectomy.

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