EFFECTS OF SEROTONIN ON SPONTANEOUS OVULATION: A THEORY FOR THE DUAL HYPOTHALAMIC CONTROL OF OVULATION

1971 ◽  
Vol 68 (2) ◽  
pp. 334-344 ◽  
Author(s):  
Anant P. Labhsetwar

ABSTRACT In an attempt to study the inhibitory effects of serotonin on spontaneous ovulation, the monoamine was administered subcutaneously to rats with 4-day oestrous cycles. Administration (50 mg/kg) at 5.00 p. m. on the day before pro-oestrus interfered with ovulation without affecting vaginal cornification, uterine ballooning or mating. This effect on ovulation could be overcome with methysergide, a specific antagonist of serotonin. Administration, at appropriate times, of LH or oestradiol benzoate or the stimulus provided by mating prevented the inhibitory effects of serotonin. implicating a central rather than a peripheral mechanism in interference with ovulation. This was further confirmed by the persistence in the serotonin-treated animals of high levels of pituitary LH, comparable to pro-oestrous levels. It is probable that serotonin blocked ovulation by augmenting the inhibitory effects of serotoninergic fibres in the hypothalamus. It is postulated on the basis of the present results and those reported in the literature that the hypothalamus exercises a dual control over ovulation, inhibitory influences being transmitted through serotonin-linked neurones while stimulatory effects are delivered via catecholaminergic fibres to neurones which synthesize releasing factor(s) for the ovulating hormone. It is postulated that a certain degree of balance in favour of the catecholaminergic system is necessary for the occurrence of ovulation. Inhibition of ovulation occurs whenever the serotoninergic system gains dominance over catecholaminergic system. The theory can account for the effects on ovulation of a multitude of chemically diverse agents reported in the literature.

1976 ◽  
Vol 82 (3) ◽  
pp. 652-660 ◽  
Author(s):  
M. F. Tarttelin ◽  
J. E. Shryne ◽  
R. A. Gorski

ABSTRACT There was no significant difference in body weight between neonatally ovariectomized (OvX) rats whether given oil treatment or 90 μg testosterone propionate (TP) on day 3, when examined up to 23 weeks of age. When these two animals were injected with oestradiol benzoate (3 μg/day for 2 weeks), the neonatally OvX TP treated rats showed a significantly smaller depression in body weight than did the control neonatally OxX rats. Measurement of food intake also showed that TP treated rats responded significantly less to the depressant effects of oestrogen than did the controls. These data are consistent with the hypothesis that the ovary does restrain body weight in TP rats but that androgen treatment in the neonatal period may not have a specific effect on growth but may alter the sensitivity of growth regulating processes to the inhibitory effects of oestrogen.


1984 ◽  
Vol 102 (2) ◽  
pp. 133-141 ◽  
Author(s):  
R. Bhanot ◽  
M. Wilkinson

ABSTRACT We have attempted to clarify the physiological involvement of endogenous opiates in the steroid-mediated control of gonadotrophin release. Our studies showed that there was an acute reduction in the inhibitory effects of endogenous opiates on LH and FSH release following gonadectomy in the rat. This was indicated by a significant reduction in the ability of naloxone to stimulate serum LH/FSH levels (sampled at 15 min) in 26-day-old female rats 48 h after ovariectomy. Luteinizing hormone was highly sensitive to the inhibitory effects of the synthetic met-enkephalin analogue, FK 33-824, at this time (sampled at 90 min). An unexpected observation was that long-term absence of gonadal steroids also disrupted the ability of exogenous opiates, FK 33-824 and morphine, to influence LH release. This was seen as an inability of FK 33-824 (1·0 or 3·0 mg/kg) to inhibit LH secretion. The effects of gonadectomy on opiate control of LH occurred at all developmental stages and were not due to a disruption of sexual maturation. Opiate involvement in prolactin secretion did not appear to be adversely affected by an absence of gonadal steroids. Another novel aspect of this work was that the opiatergic component in the control of gonadotrophin secretion could be reinstated in long-term gonadectomized rats by treatment with oestradiol benzoate or testosterone propionate. Similarly, priming with increasing dosages of oestradiol benzoate which resulted in progressively lower LH levels gave larger naloxone responses. This steroid–opiate interdependency suggests that the negative feedback influence of gonadal steroids on LH secretion is conveyed, in part, by hypothalamic opiate peptides. Our results therefore provide a neurochemical basis for gonadal steroid negative feedback. J. Endocr. (1984) 102, 133–141


1981 ◽  
Author(s):  
B Martin ◽  
C Bonne

We have recently reported that PGE2 counteracted the anti-aggregating action of PGE1 and of other PG by inhibiting the adenylate cyclase system. But this effect is not due to the interference with anti-aggregating PG receptors. In this study, the mechanism of action of the c AMPlowering effect of PGE2 has been further investigated.Suspensions of aspirin-washed human platelets were incubated for 1 min at 37°C in the presence of papaverine (0.5mM) with PGE1 , PGE2, U46619, a chemical analog of PGH2, 13-azaprostanoic acid, a specific antagonist of TxA2, either alone or in various associations. The c AMP concentration was determined by protein binding assays in platelet extracts. PGE2 (l50nM) and U46619 (1μM) inhibited the rise in c AMP induced by PGE1 (30nM) On the other hand, when 13-azaprostanoic acid (507#x03BC;M) was added to the incubate, the inhibitory effects of these compounds were suppressed.These results support the conclusion that TxA2 and U46619 act on a unique receptor which triggers the c AMP-lowering effect and suggest that PGE2 antagonizes the anti-aggregating PG through interaction with this receptor.


2000 ◽  
Vol 278 (4) ◽  
pp. E692-E699 ◽  
Author(s):  
B. Corvilain ◽  
L. Collyn ◽  
J. van Sande ◽  
J. E. Dumont

The regulation of thyroid metabolism by iodide involves numerous inhibitory effects. However, in unstimulated dog thyroid slices, a small inconstant stimulatory effect of iodide on H2O2 generation is observed. The only other stimulatory effect reported with iodide is on [1-14C]glucose oxidation, i.e., on the pentose phosphate pathway. Because we have recently demonstrated that the pentose phosphate pathway is controlled by H2O2generation, we study here the effect of iodide on basal H2O2 generation in thyroid slices from several species. Our data show that in sheep, pig, bovine, and to a lesser extent dog thyroid, iodide had a stimulatory effect on H2O2 generation. In horse and human thyroid, an inconstant effect was observed. We demonstrate in dogs that the stimulatory effect of iodide is greater in thyroids deprived of iodide, raising the possibility that differences in thyroid iodide pool may account, at least in part, for the differences between the different species studied. This represents the first demonstration of an activation by iodide of a specialized thyroid function. In comparison with conditions in which an inhibitory effect of iodide on H2O2 generation is observed, the stimulating effect was observed for lower concentrations and for a shorter incubation time with iodide. Such a dual control of H2O2 generation by iodide has the physiological interest of promoting an efficient oxidation of iodide when the substrate is provided to a deficient gland and of avoiding excessive oxidation of iodide and thus synthesis of thyroid hormones when it is in excess. The activation of H2O2 generation may also explain the well described toxic effect of acute administration of iodide on iodine-depleted thyroids.


1974 ◽  
Vol 60 (2) ◽  
pp. 205-215 ◽  
Author(s):  
L. CALIGARIS ◽  
J. J. ASTRADA ◽  
S. TALEISNIK

SUMMARY The concentration of prolactin in serum after oestrogen and progesterone injection into spayed rats was measured by radioimmunoassay. After a single injection of 5 μg oestradiol benzoate (OB) into long-term ovariectomized rats, serum prolactin concentrations showed a circadian rhythm with high levels in the afternoon and almost no changes in the morning. Peaks of prolactin occurred 2, 3 and 4 days after the injection. Below a dose of 1 μg OB, the response was dose-dependent, but the response was then maximal. In spayed rats primed with 5 μg OB, the injection of 2 mg progesterone 2, 3 or 4 days later resulted in a significant increase in serum prolactin. This response, in contrast to that of oestrogen, occurred in the morning and in the evening and was found to be dose-dependent. The rise in serum prolactin after injection of 1 mg progesterone also showed a close relationship to the priming dose of OB. Progesterone had no effect in spayed, untreated animals. Maximal levels of prolactin were attained 3–4 h after the s.c. injection of progesterone. The release of prolactin which can be induced either by OB or by progesterone was blocked by the administration of progesterone injected 1 day before the expected release would occur. These results indicate that progesterone exerts both facilitatory and inhibitory effects on prolactin secretion. Male rats were found to be less sensitive to the ovarian steroid treatment. It is suggested that oestrogen could be responsible for the rise in prolactin observed at pro-oestrus and progesterone for the increase in prolactin in pseudopregnancy and pregnancy.


2021 ◽  
Vol 12 ◽  
Author(s):  
Chao Ren ◽  
Ren-qi Yao ◽  
Li-xue Wang ◽  
Jun-cong Li ◽  
Kun-wei Chen ◽  
...  

Sepsis has emerged as a global health issue, and accounts for millions of deaths in intensive care units. Dysregulation of the immune response reportedly contributes to the pathogenesis and progression of this lethal condition, which involves both the dysfunction of immune cells and incompetent immunomodulatory mechanisms. High mobility group box 1 (HMGB1) is known as a later inflammatory mediator and is critically involved in the severity and prognosis of sepsis by inducing intractable inflammation and dysfunction of various immune cells. In the present study, we found that intracerebroventricular (ICV) injection of Box A, a specific antagonist of HMGB1, restored the dysregulated response of splenic dendritic cells (DCs) in septic mice by enhancing the expression of surface molecules, including CD80, CD86, and MHC-II, as well as improving DC priming of T lymphocytes. Cerebral HMGB1 was also confirmed to have potent inhibitory effects on DC functions when administrated by ICV injection in normal mice. The brain cholinergic system was found to mediate the immunomodulatory effects of central HMGB1, as it exhibited enhanced activity with persistent HMGB1 exposure. Furthermore, the inhibitory effects of cerebral HMGB1 on the response of peripheral DCs were also blocked by α7nAchR gene knockout. These findings provide novel insight into the relationship between cerebral HMGB1 and splenic DC dysfunction during sepsis, which is, at least in part, dependent on cholinergic system activity.


1985 ◽  
Vol 104 (3) ◽  
pp. 447-452 ◽  
Author(s):  
J. O. Willoughby ◽  
H. Pederick ◽  
P. Jervois ◽  
M. Menadue ◽  
S. J. Judd

ABSTRACT Prolactin responses to pharmacological agents were used to characterize the defect in prolactin regulation which occurs after administration of high doses of oestrogen to rats. Animals with chronically implanted venous cannulae were injected with 2 mg oestradiol benzoate in oil and 2–3 days later prolactin concentrations were measured after injections of saline, thyrotrophin-releasing hormone (TRH), fenfluramine, apomorphine and butaclamol. The responses were compared with those in oil-injected animals. Hyperprolactinaemia in oestrogen-treated animals was unresponsive to apomorphine, but was even more sensitive to dopamine receptor blockade than controls. These results suggest that the lactotrophs in oestrogen-treated animals are already maximally suppressed by endogenous dopamine, though ineffectively. Although there was an increased prolactin response to TRH in oestrogen-treated animals, there was an impaired response to fenfluramine, indicating suppressed serotonergic prolactin-releasing factor mechanisms. Maximal endogenous dopaminergic activity and suppressed prolactin-releasing factor mechanisms are appropriate hypothalamic responses to hyperprolactinaemia. The operation of these responses in the earliest stages of the development of pituitary hyperplasia indicates that oestrogen induces a disturbance of prolactin regulation in the lactotroph, independent of hypothalamic control. J. Endocr. (1985) 104, 447–452


1979 ◽  
Vol 135 (1) ◽  
pp. 162-163
Author(s):  
Karl H. Slotta

Author(s):  
Pınar Ercan ◽  
Sedef Nehir El

Abstract. The goals of this study were to determine and evaluate the bioaccessibility of total anthocyanin and procyanidin in apple (Amasya, Malus communis), red grape (Papazkarası, Vitis vinifera) and cinnamon (Cassia, Cinnamomum) using an in vitro static digestion system based on human gastrointestinal physiologically relevant conditions. Also, in vitro inhibitory effects of these foods on lipid (lipase) and carbohydrate digestive enzymes (α-amylase and α-glucosidase) were performed with before and after digested samples using acarbose and methylumbelliferyl oleate (4MUO) as the positive control. While the highest total anthocyanin content was found in red grape (164 ± 2.51 mg/100 g), the highest procyanidin content was found in cinnamon (6432 ± 177.31 mg/100 g) (p < 0.05). The anthocyanin bioaccessibilities were found as 10.2 ± 1%, 8.23 ± 0.64%, and 8.73 ± 0.70% in apple, red grape, and cinnamon, respectively. The procyanidin bioaccessibilities of apple, red grape, and cinnamon were found as 17.57 ± 0.71%, 14.08 ± 0.74% and 18.75 ± 1.49%, respectively. The analyzed apple, red grape and cinnamon showed the inhibitory activity against α-glucosidase (IC50 544 ± 21.94, 445 ± 15.67, 1592 ± 17.58 μg/mL, respectively), α-amylase (IC50 38.4 ± 7.26, 56.1 ± 3.60, 3.54 ± 0.86 μg/mL, respectively), and lipase (IC50 52.7 ± 2.05, 581 ± 54.14, 49.6 ± 2.72 μg/mL), respectively. According to our results apple, red grape and cinnamon have potential to inhibit of lipase, α-amylase and α-glucosidase digestive enzymes.


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