Effects of dopamine and morphine on immunoreactive somatostatin and LH-releasing hormone secretion from hypothalamic fragments in vitro

1985 ◽  
Vol 106 (3) ◽  
pp. 317-322 ◽  
Author(s):  
A. M. J. Lengyel ◽  
A. Grossman ◽  
P.-M. G. Bouloux ◽  
L. H. Rees ◽  
G. M. Besser
Keyword(s):  
Significant Relationship ◽  
Hormone Secretion ◽  
Progressive Increase ◽  
Releasing Hormone ◽  
Lhrh Release ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
Preincubation Medium ◽  
Hypothalamic Level

ABSTRACT Dopamine and morphine modulate GH and LH release, probably at a hypothalamic locus. To investigate this in more detail, we studied the influence of these substances on somatostatin and LH-releasing hormone (LHRH) release from rat hypothalamic fragments in vitro. Hypothalamic fragments were incubated in Earle's medium. After 60 min of preincubation, medium from two 20-min incubations was collected and somatostatin and LHRH levels measured by radioimmunoassay. Dopamine (10 nmol/l–0·1 mmol/l) induced a progressive increase (r = 0·41; P <0·01) in basal somatostatin levels. K + (30 mmol/l)-induced somatostatin release was also increased (r = 0·54; P <0·01) by increasing doses of dopamine. Metoclopramide (10 μmol/l) blocked the dopamine (1 μmol/l)-induced increase in somatostatin release. No significant relationship between dopamine and LHRH was found either basally or after K + (30 mmol/l) stimulation. Basal somatostatin was negatively correlated (r = −0·63; P <0·01) with morphine concentrations. No significant correlation was found after K+ (30 mmol/l) depolarization. Basal LHRH release was not influenced by morphine, while K +(30 mmol/l)-induced release was significantly lower than controls only at a concentration of 10 nmol/l. These results suggest that dopamine and morphine act at a hypothalamic level to modulate GH release through alterations in somatostatin secretion. Dopamine and morphine have no consistent effect on hypothalamic LHRH release. J. Endocr. (1985) 106, 317–322

Control of follicle-stimulating hormone secretion by steroid-free bovine follicular fluid in the ovariectomized rat

1983 ◽  
Vol 99 (1) ◽  
pp. 1-8 ◽  
Author(s):  
T. R. Koiter ◽  
G. C. J. van der Schaaf-Verdonk ◽  
H. Kuiper ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling
Keyword(s):  
Luteinizing Hormone ◽  
Follicular Fluid ◽  
Hormone Secretion ◽  
Ovariectomized Rats ◽  
Ovariectomized Rat ◽  
Releasing Hormone ◽  
Basal Release ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
Lh Secretion

The effects of steroid-free bovine follicular fluid (bFF) and sodium phenobarbitone on spontaneous LH releasing hormone (LHRH)-induced secretion of FSH and LH were studied in ovariectomized rats. Luteinizing hormone releasing hormone was administered by infusion to rats anaesthetized with phenobarbitone. Bovine follicular fluid reduced FSH release and synthesis. Luteinizing hormone release remained unaffected after bFF treatment. Phenobarbitone reduced both FSH and LH release. The observed suppressive effects of bFF and phenobarbitone on FSH secretion were additive, suggesting that the basal release of FSH has an LHRH-dependent and an LHRH-independent component. Furthermore, bFF did not affect pituitary responsiveness of LH secretion to LHRH and reduced the responsiveness of FSH secretion only when administered some time before the LHRH challenge. The present observations support the view that in the ovariectomized rat the pituitary gland is the only site of action of inhibin-like activity as present in bFF.

Effects of chronic treatment with oestrogen, an oestrogen antagonist and a potent luteinizing hormone releasing hormone agonist analogue on pituitary responsiveness to luteinizing hormone releasing hormone in the rat

1983 ◽  
Vol 98 (3) ◽  
pp. 313-321 ◽  
Author(s):  
J. M. Hall ◽  
S. A. Whitehead
Keyword(s):  
Luteinizing Hormone ◽  
Chronic Treatment ◽  
Ex Vivo ◽  
Significant Rise ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
Lh Releasing Hormone

The rise in gonadotrophin release which occurs after ovariectomy is caused by steroid withdrawal resulting in an enhanced pituitary responsiveness to LH releasing hormone (LHRH) associated with increased LHRH release and pituitary LHRH binding. The effects of oestrogen replacement after ovariectomy and chronic treatment of intact rats with an oestrogen antagonist, tamoxifen, on LH release and in-vitro pituitary responses to LHRH have been investigated. Capsules containing crystalline oestradiol, implanted at the time of ovariectomy, completely inhibited the rise in LH release although pituitary responsiveness was greater after 10 days in the oestrogen-treated rats than in untreated ovariectomized controls. On day 4 after ovariectomy pituitary responses to LHRH were comparable in both treated and untreated groups although in both groups the responses were greater than those measured in intact dioestrous rats. Treatment with tamoxifen over a 4-day period also augmented pituitary responsiveness but only at the lowest dose (0·5 mg/kg); no effect on serum LH concentrations was observed. Higher doses of the antagonist (1 and 2 mg/kg) did not affect pituitary responses, although the highest dose did cause a significant rise in serum LH. Treatment with a daily dose of 50 ng [d-Ser(But)6]LHRH(1–9)nonapeptide-ethylamide, starting on the day of ovariectomy, markedly attenuated the LH responses to LHRH ex vivo at days 2, 4 and 10 after ovariectomy. In contrast, the analogue treatment did not abolish the rise in LH release but this was proportionately less than in controls.

Clomiphene citrate induces luteinizing hormone release through hypothalamic luteinizing hormone-releasing hormone in vitro

1983 ◽  
Vol 103 (3) ◽  
pp. 289-292 ◽  
Author(s):  
A. Miyake ◽  
K. Tasaka ◽  
T. Sakumoto ◽  
Y. Kawamura ◽  
Y. Nagahara ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Clomiphene Citrate ◽  
Female Rats ◽  
Normal Female ◽  
Releasing Hormone ◽  
Superfusion System ◽  
In Series ◽  
Lh Release ◽  
Lh Releasing Hormone

Abstract. The releasing effects of clomiphene citrate (clomiphene) on luteinizing hormone (LH) and LH-releasing hormone (LRH) were examined in a sequential double chamber superfusion system by superfusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were superfused in sequence with medium containing 2 × 10−10 m oestradiol (E2), two significant peaks in LH release (60–130% increase, P < 0.05) were observed 40 min and 90 min after the administration of 3 × 10−8 mol clomiphene. Administration of clomiphene in medium without E2 induced a low peak (25–50% increase, P < 0.05) of LH released from the pituitary perfused in series with the MBH. Administration of clomiphene did not cause a marked increase of LH from the pituitary superfused alone, when superfused with or without E2 containing medium. The concentration of LRH in the efflux was significantly increased (50–100%) 40 min and 90 min after clomiphene administration when MBH was superfused with medium containing E2, whereas clomiphene had no effect when superfused with medium alone. These data indicate: 1) that clomiphene induces LRH release from the MBH, that it may induce LH release, in part, by acting directly at the pituitary level; 2) that changes in LH after clomiphene administration coincide with LRH release, and 3) that a certain concentration of E2 may be necessary for the secretion of LRH by clomiphene.

scholarly journals α1-Adrenergic Receptors Mediate LH-Releasing Hormone Secretion through Phospholipases C and A2 in Immortalized Hypothalamic Neurons

Endocrinology ◽  
2001 ◽  
Vol 142 (11) ◽  
pp. 4839-4851 ◽  
Author(s):  
Silvia M. Kreda ◽  
Martina Sumner ◽  
Silvia Fillo ◽  
Carla M. Ribeiro ◽  
Guo X. Luo ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Critical Role ◽  
Hormone Secretion ◽  
Receptor Activation ◽  
Dependent Manner ◽  
Adrenergic Agents ◽  
Releasing Hormone ◽  
Lh Releasing Hormone

Abstract Norepinephrine has long been known to stimulate the pulsatile and preovulatory release of LH-releasing hormone (LHRH). In vivo and in vitro studies indicate that these effects are mediated primarily through α1-adrenergic receptors (α1-ARs). With the immortalized hypothalamic LHRH neurons, we have found that α1-adrenergic agents directly stimulate the secretion of LHRH in a dose-dependent manner. Ligand binding and RNA studies demonstrate that the GT1 cells contain both α1A- and α1B-ARs. Competition binding experiments show that approximately 75% of the binding is due toα 1B-ARs; the remainder is made up ofα 1A-ARs. Receptor activation leads to stimulation of PLC. PLCβ1 and PLCβ3 are expressed in GT1 neurons, and these PLCs are probably responsible for the release of diacylglycerol and IP as well as the increase in intracellular calcium. The mobilization of cytoplasmic calcium is sufficient to stimulate cytosolic PLA2 (cPLA2) and release arachidonic acid. A dissection of the contributions of the phospholipases to LHRH secretion suggests that cPLA2 acts downstream of PLC and that it significantly augments the PLC-stimulated LHRH secretory response. Inasmuch as the α1-ARs are known to play a critical role in LHRH physiology, we propose that both PLC and cPLA2 are critical in regulating and amplifying LHRH release.

Hydrocortisone elicits the effect of clomiphene citrate on luteinizing hormone-releasing hormone release in vitro

1984 ◽  
Vol 107 (2) ◽  
pp. 145-148 ◽  
Author(s):  
Akira Miyake ◽  
Keiichi Tasaka ◽  
Tetsuro Sakumoto ◽  
Yasuhito Nagahara ◽  
Toshihiro Aono
Keyword(s):  
Luteinizing Hormone ◽  
Clomiphene Citrate ◽  
Female Rats ◽  
Normal Female ◽  
Releasing Hormone ◽  
In Series ◽  
Significant Release ◽  
Lh Release ◽  
Lh Releasing Hormone

Abstract. The effect of hydrocortisone on the release of luteinizing hormone (LH) and LH-releasing hormone (LRH) in response to clomiphene citrate (clomiphene) were examined in a sequential double chamber perifusion system by perifusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were perifused in sequence with medium containing 5 × 10−6 m hydrocortisone, a significant release in LH (100– 150% increase, P < 0.01–P < 0.05) was observed 40 min after the administration of 3 × 10−8 mol clomiphene. Clomiphene had no effect on LH release from the pituitary when perifused in series with the MBH without basal hydrocortisone infusion. Administration of clomiphene did not cause a significant increase in LH from the pituitary perifused alone, with or without medium containing hydrocortisone. The concentration of LRH in the efflux was significantly increased 40 min after clomiphene administration when MBH was perifused with medium containing hydrocortisone, whereas clomiphene had no effect when perifused with medium only. These data indicate that hydrocortisone stimulates the effect of clomiphene on LRH release from the hypothalamus, which in turn induces LH release from the pituitary.

IMMATURE RAT PITUITARY GLANDS IN VITRO: AGE- AND SEX-RELATED CHANGES IN LUTEINIZING HORMONE RELEASING HORMONE-STIMULATED GONADOTROPHIN RELEASE

1977 ◽  
Vol 73 (2) ◽  
pp. 309-319 ◽  
Author(s):  
J. DULLAART
Keyword(s):  
Male Rats ◽  
Steady Increase ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Lh Release ◽  
The One ◽  
Lh Rh ◽  
Lh Releasing Hormone

SUMMARY Pituitary glands from immature female and male rats aged between 5 and 30 days were incubated in vitro and the effect of LH releasing hormone (RH) on the release of LH and FSH was studied. Pituitary gonadotrophin contents were also measured. Gonadotrophin release showed changes with age as well as sex differences: after LH-RH stimulation the female pattern of release of LH and FSH (expressed per mg pituitary tissue) showed a peak at day 15; the male pattern of LH release was characterized by a steady increase with age, whereas FSH release stayed more or less constant from day 10 onwards. In both sexes the LH:FSH ratio increased with age, both in pituitary gonadotrophin content and in the mixture of gonadotrophins released. It is discussed, that the prepubertal development of pituitary gonadotrophic function might be determined on the one hand by rather autonomous growth processes (more or less similar in female and male hypophyses) and on the other hand by modulating influences of sex steroid hormones, which are different in female and male animals.

Rhythmicity of luteinizing hormone secretion expressed in vitro

1996 ◽  
Vol 135 (4) ◽  
pp. 455-463 ◽  
Author(s):  
Hadas Lewy ◽  
Zvi Naor ◽  
Israel E Ashkenazi
Keyword(s):  
Luteinizing Hormone ◽  
Human Genetics ◽  
Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone ◽  
Tel Aviv ◽  
Hypothalamic Control ◽  
Lh Release

Lewy H, Naor Z, Ashkenazi IE. Rhythmicity of luteinizing hormone secretion expressed in vitro. Eur J Endocrinol 1996;135:455–63. ISSN 0804–4643 In the present study we explored the possibility that the pituitary functions as an autonomous clock and is capable of generating rhythms of luteinizing hormone (LH) release independently of hypothalamic control. Pituitaries from estrous or diestrous day 1 female mice were perifused separately with Medium-199. Effluent samples were collected at 10-min intervals and assayed for LH levels. Fourier analysis and curve-fit analysis served to elucidate the presence of prominent periods whose significance was then determined by best-fit cosinor. The latter method was used to determine additional parameters for the significant rhythm. All perifused pituitaries exhibited LH release patterns that were composed of significantly long ultradian rhythms (approximately 16 and 8 h, p < 0.001). Continuous stimulation with gonadotropin-releasing hormone (GnRH) or estradiol did not alter the periods of the observed rhythms but affected other rhythm parameters. Gonadotropin-releasing hormone increased the mesor of the rhythm and estradiol increased the amplitude. The results indicate that pituitary gonadotropes are capable of producing rhythms of LH release for a long duration in vitro, in the absence of hypothalamic control. Both GnRH and estradiol affect different rhythm parameters but do not change the periods of these rhythms. Israel E Ashkenazi, Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel

Reproductive hormone secretion and spermatogenic function in thyroidectomized rams receiving graded doses of exogenous thyroxine

1986 ◽  
Vol 111 (2) ◽  
pp. 245-253 ◽  
Author(s):  
Y. Chandrasekhar ◽  
M. J. D'Occhio ◽  
B. P. Setchell
Keyword(s):  
Hormone Secretion ◽  
Reproductive Function ◽  
Pulse Frequency ◽  
Endocrine Function ◽  
Sex Hormone Binding Globulin ◽  
Testosterone Levels ◽  
Reproductive Endocrine ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
The Relationship

ABSTRACT This study aimed to obtain a better understanding of the relationship between circulating thyroxine (T4) concentrations and reproductive endocrine function in the ram. Mature Merino rams were thyroidectomized and supplemented with 0, 30, 100 and 300% of normal T4 for 10 weeks. Thyroidectomy had no apparent effect on spermatogenic function but interfered with sperm maturation, the latter being returned to normal by 30% T4 replacement. Circulating testosterone levels were reduced by thyroidectomy and restored to control levels by 30% T4; when T4 levels were supranormal (300%), circulating testosterone levels were again reduced. The lowered circulating testosterone levels in thyroidectomized rams occurred as a result of suppressed testosterone secretion from the testis, observed under basal conditions and also following LH-releasing hormone (LHRH) and human chorionic gonadotrophin injection. In thyroidectomized rams, sex hormone binding globulin (SHBG) levels were depressed without changes in testosterone clearance rate (TCR), while in rams with supranormal T4 levels, TCR was increased without changes in SHBG levels. Subnormal levels of T4 also restored to normal the reduced LH pulse frequency in thyroidectomized rams. Reduced LH pulse frequency, together with diminished LH release following LHRH injection in thyroidectomized rams, suggested effects of T4 at the hypothalamo-pituitary axis. The present study demonstrates that complete lack of thyroid hormones suppresses normal reproductive endocrine function in the ram, but that this can be restored to normal by 30% T4 replacement. The results support the theory that T4 plays a permissive rather than a regulatory role in reproductive function in males. J. Endocr. (1986) 111, 245–253

Sign in / Sign up

Export Citation Format

Share Document