Changes in pituitary responsiveness to LH-releasing hormone after acute buserelin treatment: a time-course and dose–response study

1985 ◽  
Vol 106 (1) ◽  
pp. 27-30 ◽  
Author(s):  
J. D. Heather ◽  
S. A. Whitehead
Keyword(s):  
Time Course ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Significant Difference ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
In Vivo Effects ◽  
Dose Response Study

ABSTRACT The acute in-vivo effects of a potent LH-releasing hormone (LHRH) agonist, buserelin, on LH secretion and pituitary responsiveness to LHRH have been investigated in oestrous rats. Doses of 50, 100 and 250 ng buserelin stimulated LH release in a dose-dependent manner, the peak serum LH concentrations being measured 1 h after the treatment. Thereafter LH levels fell rapidly between 1 and 6 h and by 18 h serum LH concentrations were similar in all groups of animals. Pituitary responsiveness to a challenge with 100 ng LHRH was potentiated by 50 or 100 ng buserelin injected 1 or 2 h before the LHRH challenge. In contrast, 250 ng buserelin completely abolished the LH response to LHRH when tested 1, 2 and 4 h after treatment, but by 6 h a small but attenuated response was observed. Four hours after treatment there was no significant difference in the responses when compared with the saline-treated controls. J. Endocr. (1985) 106, 27–30

Effects of crude and highly purified bovine inhibin (Mr 32 000 form) on gonadotrophin production by ovine pituitary cells in vitro: inhibin enhances gonadotrophin-releasing hormone-induced release of LH

1990 ◽  
Vol 127 (1) ◽  
pp. 149-159 ◽  
Author(s):  
S. Muttukrishna ◽  
P. G. Knight
Keyword(s):  
Primary Cultures ◽  
Suppressive Effect ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

ABSTRACT Primary cultures of ovine pituitary cells (from adult ewes) were used to investigate the actions of steroid-free bovine follicular fluid (bFF) and highly-purified Mr 32 000 bovine inhibin on basal and gonadotrophin-releasing hormone (GnRH)-induced release of FSH and LH. Residual cellular contents of each hormone were also determined allowing total gonadotrophin content/well to be calculated. As in rats, both crude and highly purified inhibin preparations promoted a dose (P < 0·001)- and time (P < 0·001)-dependent suppression of basal and GnRH-induced release of FSH as well as an inhibition of FSH synthesis, reflected by a fall in total FSH content/well. However, while neither inhibin preparation affected basal release of LH or total LH content/well, GnRH-induced LH release was significantly (P< 0·001) increased by the presence of either bFF (+ 75%) or highly-purified inhibin (+ 64%) in a dose- and time-dependent manner. This unexpected action of bFF on GnRH-induced LH release was abolished in the presence of 5 μl specific anti-inhibin serum, confirming that the response was indeed mediated by inhibin. Furthermore, neither oestradiol-17β (1 pmol/l–10 nmol/l) nor monomeric α-subunit of bovine inhibin (2·5–40 ng/ml) significantly affected basal or GnRH-induced release of LH. These in-vitro findings for the ewe lend support to a number of recent in-vivo observations and indicate that, in addition to its well-documented suppressive effect on the synthesis and secretion of FSH, inhibin may actually facilitate LH release in this species, in marked contrast to its action in the rat. Journal of Endocrinology (1990) 127, 149–159

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.

Testosterone metabolites do not participate in the control of hypothalamic LH-releasing hormone

1986 ◽  
Vol 109 (2) ◽  
pp. 291-296 ◽  
Author(s):  
M. Zanisi ◽  
F. Celotti ◽  
P. Ferraboschi ◽  
M. Motta
Keyword(s):  
Testosterone Propionate ◽  
Male Rats ◽  
Free Form ◽  
Releasing Hormone ◽  
Specific Radioimmunoassay ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Testosterone Metabolites ◽  
Lh Releasing Hormone

ABSTRACT To determine whether the ability of testosterone to increase intrahypothalamic LH-releasing hormone (LHRH) in orchidectomized rats might be explained by the conversion of the hormone into either its 5α-reduced or oestrogenic metabolites, testosterone, 5α-androstan-17β-ol-3-one (DHT), 5α-androstane-3α, 17β-diol (3α-diol) and 5α-androstane-3β,17β-diol (3β-diol) (2 mg/rat per day for 6 days) and oestradiol (0·1, 0·5, 1·0 and 5·0 μg/rat per day for 6 days) were injected into castrated male rats. After 6 days the rats were killed and serum LH levels and intrahypothalamic LHRH stores measured using specific radioimmunoassay procedures. Testosterone and its 5α-reduced metabolites were used in either the free alcohol or the propionate form (dipropionates in the case of the diols); oestradiol was used as oestradiol-17β or in the benzoate form. Treatment with testosterone, DHT, 3α-diol and 3β-diol resulted in a significant decrease in serum LH levels; all the 5α-reduced testosterone derivatives were more effective than testosterone in this respect. Testosterone and DHT propionates suppressed LH release following orchidectomy totally; 3α-diol and 3β-diol dipropionates were less effective. Testosterone increased intrahypothalamic LHRH stores, this effect being much higher after testosterone propionate, i.e. when intrahypothalamic LHRH stores were restored to pre-castration levels. None of the 5α-reduced steroids was capable of modifying the low intrahypothalamic levels of LHRH found following orchidectomy; only 3α-diol dipropionate exhibited some activity, but this was much lower than that of testosterone propionate. Oestradiol-17β was totally ineffective in decreasing serum LH in orchidectomized animals; in contrast, oestradiol benzoate progressively decreased serum LH. Oestradiol in the free form was unable to increase LHRH stores, as was oestradiol benzoate except at the highest dose. The results suggest that the effect exerted by testosterone on hypothalamic LHRH is due to the hormone as such and does not involve its conversion into either 5α-reduced or oestrogenic metabolites. J. Endocr. (1986) 109, 291–296

In vitro and in vivo effects of ghrelin on luteinizing hormone and growth hormone release in goldfish

2004 ◽  
Vol 286 (6) ◽  
pp. R1093-R1101 ◽  
Author(s):  
Suraj Unniappan ◽  
Richard E. Peter
Keyword(s):  
Growth Hormone ◽  
Luteinizing Hormone ◽  
Mrna Expression ◽  
Pituitary Cells ◽  
The Novel ◽  
Serum Lh ◽  
Lh Release ◽  
In Vivo Effects

We studied the in vitro and in vivo effects of octanoylated goldfish ghrelin peptides (gGRL-19 and gGRL-12) on luteinizing hormone (LH) and growth hormone (GH) release in goldfish. gGRL-19 and gGRL-12 at picomolar doses stimulated LH and GH release from dispersed goldfish pituitary cells in perifusion and static incubation. Incubation of pituitary cells for 2 h with 10 nM gGRL-12 and 1 or 10 nM gGRL-19 increased LH-β mRNA expression, whereas only 10 nM gGRL-19 increased GH mRNA expression. Somatostatin-14 abolished the stimulatory effects of ghrelin on GH release from dispersed pituitary cells in perifusion and static culture. The GH secretagogue receptor antagonist d-Lys3-GHRP-6 inhibited the ghrelin-induced LH release, whereas no effects were found on stimulation of GH release by ghrelin. Intracerebroventricular injection of 1 ng/g body wt of gGRL-19 or intraperitoneal injection of 100 ng/g body wt of gGRL-19 increased serum LH levels at 60 min after injection, whereas significant increases in GH levels were found at 15 and 30 min after these treatments. Our results indicate that, in addition to its potent stimulatory actions on GH release, goldfish ghrelin peptides have the novel function of stimulating LH release in goldfish.

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.

Dissociation Between LH Release and Pituitary Cyclic Nucleotide Accumulation in Response to Synthetic LH-Releasing Hormone in vivo

1976 ◽  
Vol 20 (1) ◽  
pp. 35-42 ◽  
Author(s):  
A. Ratner ◽  
M.C. Wilson ◽  
L. Srivastava ◽  
G.T. Peake
Keyword(s):  
Cyclic Nucleotide ◽  
Releasing Hormone ◽  
Lh Release ◽  
Lh Releasing Hormone

EFFECT OF CORTISOL OR ADRENOCORTICOTROPHIN ON RELEASE OF LUTEINIZING HORMONE INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE IN THE DAIRY HEIFER

1982 ◽  
Vol 92 (1) ◽  
pp. 141-146 ◽  
Author(s):  
R. L. MATTERI ◽  
G. P. MOBERG
Keyword(s):  
Luteinizing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Dairy Heifers ◽  
Significant Difference ◽  
Significant Depression ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
And Control ◽  
Slight Depression

During treatment with cortisol or ACTH, dairy heifers were given two doses of LH releasing hormone (LH-RH) spaced 1·5 h apart. Serum concentrations of cortisol and LH were monitored during each treatment. Treatment with both ACTH and cortisol raised plasma cortisol levels above the respective saline controls (P<0·001). Neither treatment affected basal LH concentrations. A slight depression in LH response was seen in the cortisol-treated animals after the first LH-RH injection, as shown by a statistically significant depression at three of the sample times. There was no significant difference between treated and control LH values after the second LH-RH administration. Treatment with ACTH resulted in significantly reduced LH values at all sample times after both injections of LH-RH.

scholarly journals Decoding the temporal nature of brain GR activity in the NFκB signal transition leading to depressive-like behavior

2021 ◽  
Author(s):  
Young-Min Han ◽  
Min Sun Kim ◽  
Juyeong Jo ◽  
Daiha Shin ◽  
Seung-Hae Kwon ◽  
...  
Keyword(s):  
Inhibitory Action ◽  
Time Course ◽  
Molecular Mechanisms ◽  
Late Phase ◽  
Fine Tuning ◽  
Dependent Manner ◽  
Middle Phase ◽  
Temporal Shift

AbstractThe fine-tuning of neuroinflammation is crucial for brain homeostasis as well as its immune response. The transcription factor, nuclear factor-κ-B (NFκB) is a key inflammatory player that is antagonized via anti-inflammatory actions exerted by the glucocorticoid receptor (GR). However, technical limitations have restricted our understanding of how GR is involved in the dynamics of NFκB in vivo. In this study, we used an improved lentiviral-based reporter to elucidate the time course of NFκB and GR activities during behavioral changes from sickness to depression induced by a systemic lipopolysaccharide challenge. The trajectory of NFκB activity established a behavioral basis for the NFκB signal transition involved in three phases, sickness-early-phase, normal-middle-phase, and depressive-like-late-phase. The temporal shift in brain GR activity was differentially involved in the transition of NFκB signals during the normal and depressive-like phases. The middle-phase GR effectively inhibited NFκB in a glucocorticoid-dependent manner, but the late-phase GR had no inhibitory action. Furthermore, we revealed the cryptic role of basal GR activity in the early NFκB signal transition, as evidenced by the fact that blocking GR activity with RU486 led to early depressive-like episodes through the emergence of the brain NFκB activity. These results highlight the inhibitory action of GR on NFκB by the basal and activated hypothalamic-pituitary-adrenal (HPA)-axis during body-to-brain inflammatory spread, providing clues about molecular mechanisms underlying systemic inflammation caused by such as COVID-19 infection, leading to depression.

scholarly journals Uptake and Distribution of Administered Bone Marrow Mesenchymal Stem Cell Extracellular Vesicles in Retina

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 730
Author(s):  
Biji Mathew ◽  
Leianne A. Torres ◽  
Lorea Gamboa Gamboa Acha ◽  
Sophie Tran ◽  
Alice Liu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Extracellular Vesicles ◽  
Time Course ◽  
Ganglion Cells ◽  
Ex Vivo ◽  
Dependent Manner ◽  
Paracrine Effects

Cell replacement therapy using mesenchymal (MSC) and other stem cells has been evaluated for diabetic retinopathy and glaucoma. This approach has significant limitations, including few cells integrated, aberrant growth, and surgical complications. Mesenchymal Stem Cell Exosomes/Extracellular Vesicles (MSC EVs), which include exosomes and microvesicles, are an emerging alternative, promoting immunomodulation, repair, and regeneration by mediating MSC’s paracrine effects. For the clinical translation of EV therapy, it is important to determine the cellular destination and time course of EV uptake in the retina following administration. Here, we tested the cellular fate of EVs using in vivo rat retinas, ex vivo retinal explant, and primary retinal cells. Intravitreally administered fluorescent EVs were rapidly cleared from the vitreous. Retinal ganglion cells (RGCs) had maximal EV fluorescence at 14 days post administration, and microglia at 7 days. Both in vivo and in the explant model, most EVs were no deeper than the inner nuclear layer. Retinal astrocytes, microglia, and mixed neurons in vitro endocytosed EVs in a dose-dependent manner. Thus, our results indicate that intravitreal EVs are suited for the treatment of retinal diseases affecting the inner retina. Modification of the EV surface should be considered for maintaining EVs in the vitreous for prolonged delivery.

Role of Apolipoprotein A-I in Protecting against Endotoxin Toxicity

2004 ◽  
Vol 36 (6) ◽  
pp. 419-424 ◽  
Author(s):  
Juan Ma ◽  
Xue-Ling Liao ◽  
Bin Lou ◽  
Man-Ping Wu
Keyword(s):  
Survival Time ◽  
Binding Capacity ◽  
Density Lipoprotein ◽  
Mtt Method ◽  
Apolipoprotein A ◽  
Plasma Fraction ◽  
Significant Difference ◽  
In Vivo Effects

Abstract High density lipoprotein (HDL) binds lipopolysaccharide (LPS or endotoxin) and neutralizes its toxicity. We investigated the function of Apolipoprotein A-I (ApoA-I), a major apolipoprotein in HDL, in this process. Mouse macrophages were incubated with LPS, LPS+ApoA-I, LPS+ApoA-I+LFF (lipoprotein-free plasma fraction d>1.210 g/ml), LPS+HDL, LPS+HDL+LFF, respectively. MTT method was used to detect the mortality of L-929 cells which were attacked by the release-out cytokines in LPS-activated macrophages. It was found that ApoA-I significantly decreased L-929 cells mortality caused by LPS treatment (LPS vs. LPS+ApoA-I, P<0.05) and this effect became even more significant when LFF was utilized (LPS vs. LPS+ApoA-I+LFF, P<0.01; LPS vs. LPS+HDL+LFF, P<0.01). There was no significant difference between LPS+ApoA-I+LFF and LPS+HDL+LFF treatment, indicating that ApoA-I was the main factor. We also investigated in vivo effects of ApoA-I on mouse mortality rate and survival time after LPS administration. We found that the mortality in LPS+ApoA-I group (20%) and in LPS+ApoA-I+LFF group (10%) was significantly lower than that in LPS group (80%) (P<0.05, P<0.01, respectively); the survival time was (43.20 ± 10.13) h in LPS+ApoA-I group and (46.80 ± 3.79) h in LPS+ApoA-I+LFF group, which were significantly longer than that in LPS group (16.25 ± 17.28) h (P<0.01). We also carried out in vitro binding study to investigate the binding capacity of ApoA-I and ApoA-I+LFF to fluorescence labeled LPS (FITC-LPS). It was shown that both ApoA-I and ApoA-I+LFF could bind with FITC-LPS, however, the binding capacity of ApoA-I+LFF to FITC-LPS (64.47 ± 8.06) was significantly higher than that of ApoA-I alone (24.35 ± 3.70) (P<0.01). The results suggest that: (1) ApoA-I has the ability to bind with and protect against LPS; (2) LFF enhances the effect of ApoA-I; (3) ApoA-I is the major contributor for HDL anti-endotoxin function.

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