scholarly journals Peripheral Inhibitor of AChE, Neostigmine, Prevents the Inflammatory Dependent Suppression of GnRH/LH Secretion during the Follicular Phase of the Estrous Cycle

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Andrzej P. Herman ◽  
Janina Skipor ◽  
Agata Krawczyńska ◽  
Joanna Bochenek ◽  
Karolina Wojtulewicz ◽  
...  
Keyword(s):  
Estrous Cycle ◽  
Inhibitory Effect ◽  
Follicular Phase ◽  
Ache Inhibitor ◽  
Ache Inhibitors ◽  
The Central Nervous System ◽  
Lh Release ◽  
Hypothalamic Structure ◽  
Lh Secretion ◽  
Lps Treatment

The study was designed to test the hypothesis that the inhibition of acetylcholinesterase (AChE) activity at the periphery by Neostigmine (0.5 mg/animal) will be sufficient to prevent inflammatory dependent suppression of the gonadotropin-releasing hormone (GnRH)/luteinising hormone (LH) secretion in ewes in the follicular phase of the estrous cycle, and this effect will be comparable with the systemic AChE inhibitor, Donepezil (2.5 mg/animal). An immune/inflammatory challenge was induced by peripheral administration of lipopolysaccharide (LPS; 400 ng/kg). Peripheral treatment with Donepezil and Neostigmine prevented the LPS-induced decrease (P<0.05) in LHβ gene expression in the anterior pituitary gland (AP) and in LH release. Moreover, Donepezil completely abolished (P<0.05) the suppressory effect of inflammation on GnRH synthesis in the preoptic area, when pretreatment with Neostigmine reduced (P<0.05) the decrease in GnRH content in this hypothalamic structure. Moreover, administration of both AChE inhibitors diminished (P<0.05) the inhibitory effect of LPS treatment on the expression of GnRH receptor in the AP. Our study shows that inflammatory dependent changes in the GnRH/LH secretion may be eliminated or reduced by AChE inhibitors suppressing inflammatory reaction only at the periphery such as Neostigmine, without the need for interfering in the central nervous system.

scholarly journals Neostigmine Attenuates Proinflammatory Cytokine Expression in Preoptic Area but Not Choroid Plexus during Lipopolysaccharide-Induced Systemic Inflammation

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Andrzej P. Herman ◽  
Dorota Tomaszewska-Zaremba ◽  
Marta Kowalewska ◽  
Aleksandra Szczepkowska ◽  
Małgorzata Oleszkiewicz ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Proinflammatory Cytokine ◽  
Preoptic Area ◽  
De Novo ◽  
Brain Parenchyma ◽  
Ache Inhibitor ◽  
Ache Inhibitors ◽  
Reproduction Process ◽  
Hypothalamic Structure ◽  
Alpha 7

The study was designed to examine whether the administration of neostigmine (0.5 mg/animal), a peripheral inhibitor of acetylcholinesterase (AChE), during an immune/inflammatory challenge provoked by intravenous injection of bacterial endotoxin—lipopolysaccharide (LPS; 400 ng/kg)—attenuates the synthesis of proinflammatory cytokines in the ovine preoptic area (POA), the hypothalamic structure playing an essential role in the control of the reproduction process, and in the choroid plexus (CP), a multifunctional organ sited at the interface between the blood and cerebrospinal fluid in the ewe. Neostigmine suppressed (p<0.05) LPS-stimulated synthesis of cytokines such as interleukin- (IL-) 1β, IL-6, and tumor necrosis factor (TNF) α in the POA, and this effect was similar to that induced by the treatment with systemic AChE inhibitor—donepezil (2.5 mg/animal). On the other hand, both AChE inhibitors did not influence the gene expression of these cytokines and their corresponding receptors in the CP. It was found that this structure seems to not express the neuronal acetylcholine (ACh) receptor subunit alpha-7, required for anti-inflammatory action of ACh. The mechanism of action involves inhibition of the proinflammatory cytokine synthesis on the periphery as well as inhibition of their de novo synthesis rather in brain microvessels and not in the CP. In conclusion, it is suggested that the AChE inhibitors incapable of reaching brain parenchyma might be used in the treatment of neuroinflammatory processes induced by peripheral inflammation.

Plasma β-endorphin and LH during prolonged hypoglycaemia in ewes

1993 ◽  
Vol 1993 ◽  
pp. 93-93 ◽  
Author(s):  
A.M.X. Eloy ◽  
R.G. Rodway
Keyword(s):  
Plasma Concentrations ◽  
Reproductive Function ◽  
Opioid Peptide ◽  
Inhibitory Effect ◽  
Elevated Plasma ◽  
Lh Release ◽  
Lh Secretion

Normal reproductive function in female animals can be drastically impaired by a variety of stressful stimuli. For example, undernutrition and hypoglycaemia in sheep have been shown to suppress pulsatile LH secretion and to reduce the number of ewes showing pre-ovulatory LH peaks (Crump and Rodway 1986, Clarke et al. 1990). Similar stresses are also known to cause release of the opioid peptide β-endorphin into the circulation. Opioids are well-known to have a central inhibitory effect on LH release, although whether the elevated plasma concentrations of these peptides have any effect on LH secretion is unclear. The present study investigated the affect of insulin-induced hypoglycaemia on plasma concentrations of β-endorphin and LH.

The effect of rivastigmine on the LPS-induced suppression of GnRH/LH secretion during the follicular phase of the estrous cycle in ewes

2013 ◽  
Vol 138 (3-4) ◽  
pp. 203-212 ◽  
Author(s):  
A.P. Herman ◽  
A. Krawczyńska ◽  
J. Bochenek ◽  
K. Haziak ◽  
K. Romanowicz ◽  
...  
Keyword(s):  
Estrous Cycle ◽  
Follicular Phase ◽  
Lh Secretion

Evidence for an increased opioid inhibition of LH secretion in hyperprolactinaemic ovariectomized rats

1984 ◽  
Vol 101 (1) ◽  
pp. 57-61 ◽  
Author(s):  
D. A. Carter ◽  
J. S. Cooper ◽  
S. E. Inkster ◽  
S. A. Whitehead
Keyword(s):  
Positive Feedback ◽  
Day Treatment ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Dopamine Antagonist ◽  
Similar Treatment ◽  
Lh Surge ◽  
Lh Release ◽  
Ovine Prolactin ◽  
Lh Secretion

ABSTRACT The effects of acute and sub-chronic hyperprolactinaemia on the positive feedback action of progesterone in oestrogen-primed ovariectomized rats have been compared. A single injection of ovine prolactin administered with progesterone had no effect on the LH surge measured 5 h later although hyperprolactinaemia induced by 5-day treatment with the dopamine antagonist, domperidone, markedly attenuated the surge. Repeated injections of naloxone (5 mg/kg) during the development of the progesterone-stimulated LH surge completely reversed this inhibitory effect of hyperprolactinaemia, but had no apparent effect on the positive feedback action in control animals. In oestrogen-primed animals similar treatment with naloxone (0·4 and 5 mg/kg) stimulated LH secretion but the increase was significantly smaller than that observed after injecting progesterone. It is suggested that hyperprolactinaemia increases the inhibitory opioid modulation of LH release and that this effect is responsible for the impairment of the positive feedback action of progesterone. J. Endocr. (1984) 101, 57–61

Prolactin- and testosterone-induced inhibition of LH secretion after orchidectomy: role of catecholaminergic neurones terminating in the diagonal band of Broca, medial preoptic nucleus and median eminence

1996 ◽  
Vol 148 (2) ◽  
pp. 291-301 ◽  
Author(s):  
S-K Park ◽  
D A Strouse ◽  
M Selmanoff
Keyword(s):  
Median Eminence ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Testosterone Replacement ◽  
Preoptic Nucleus ◽  
Medial Preoptic Nucleus ◽  
Diagonal Band ◽  
Lh Release ◽  
Diagonal Band Of Broca ◽  
Lh Secretion

Abstract Central catecholaminergic neurones projecting to specific hypothalamic structures are involved in stimulating and inhibiting the activity of the GnRH-containing neurosecretory neurones. Both testosterone and elevated circulating prolactin (PRL) levels inhibit postcastration LH release. Three groups of adult male rats were orchidectomized and adrenalectomized, received corticosterone replacement and were: (i) administered purified ovine PRL (oPRL; 2400 μg/s.c. injection) or (ii) its diluent, polyvinylpyrrolidone (PVP), every 12 h, or (iii) received physiological testosterone replacement for 2 days. At 0, 2 and 6 days postcastration, norepinephrine (NE), epinephrine (E) and dopamine (DA) turnover were estimated by the α-methyl-p-tyrosine method in three micro-dissected hypothalamic structures: the diagonal band of Broca at the level of the organum vasculosum of the lamina terminalis (DBB(ovlt)), the medial preoptic nucleus (MPN) and the median eminence (ME). In control (PVP-treated) rats, serum LH concentrations increased eightfold at 2 and 6 days postcastration and this rise was prevented by testosterone. oPRL treatment transiently suppressed LH secretion at 2 but not 6 days postcastration. Castration significantly decreased basal rat PRL (rPRL) levels at 2 and 6 days and testosterone administration partially prevented this effect. NE turnover in the ME and E turnover in the MPN increased markedly at 2 and 6 days postcastration, and testosterone replacement for 2 days prevented these increases. Thus, noradrenergic neurones innervating the ME and adrenergic neurones innvervating the MPN may drive postcastration LH secretion by providing stimulatory afferent input to the GnRH neurones. It was striking to observe that oPRL blocked the increases in both ME NE and MPN E turnover at 2 but not 6 days postcastration. Hence, oPRL may transiently suppress LH release by an inhibitory action on these NE and E neurones. DA turnover in the DBB(ovlt) was significantly decreased by 6 days postcastration. Testosterone-treated (2 days postcastration) and oPRL-treated (2 and 6 days postcastration) rats exhibited turnover values indistinguishable from day 0 controls. Hence, the A14 dopaminergic neurones, which synapse on GnRH neurones in the rostral preoptic area and may exert an inhibitory effect on them, are positively regulated by PRL and perhaps by testosterone as well. Autoregulatory feedback suppression of endogenous rPRL secretion by oPRL was observed both 2 and 6 days postcastration. In contrast to the A14 dopaminergic neurones, turnover in the A12 tuberoinfundibular dopaminergic (TIDA) neurones innervating the ME increased significantly by 6 days postcastration in control rats while oPRL administration further increased ME DA turnover at both 2 and 6 days. Hence, autofeedback regulation of rPRL secretion persists through at least 6 days of oPRL exposure temporally associated with markedly increased turnover in the TIDA neurones. In summary, our results support the hypothesis that the inhibitory effect of PRL on postcastration LH release is mediated by suppression of the activity of NE neurones innervating the ME and E neurones terminating in the MPN which, with time, become refractory to continued PRL exposure. Journal of Endocrinology (1996) 148, 291–301

scholarly journals Ovarian stimulation with FSH reduces phosphorylation of gonadotrope progesterone receptor and LH secretion in the rat

Reproduction ◽  
2009 ◽  
Vol 137 (1) ◽  
pp. 151-159 ◽  
Author(s):  
Ana Gordon ◽  
José C Garrido-Gracia ◽  
Rafaela Aguilar ◽  
Silvia Guil-Luna ◽  
Yolanda Millán ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Ovarian Stimulation ◽  
Inhibitory Effect ◽  
Ovx Rats ◽  
Formalin Fixed Paraffin ◽  
Formalin Fixed Paraffin Embedded ◽  
Experimental Approaches ◽  
Lh Release ◽  
Lh Secretion

Administration of human FSH (hFSH) to cyclic rats during the dioestrous phase attenuates progesterone receptor (PR)-dependent events of the preovulatory LH surge in pro-oestrus. The increased bioactivity of the putative ovarian gonadotropin surge inhibiting/attenuating factor induced by hFSH treatment is not associated with a decrease in PR protein expression, and the possibility of its association at a PR posttranslational effect has been raised. The present experiments aimed to analyse PR phosphorylation status in the gonadotrope of rats with impaired LH secretion induced byin vivohFSH injection. Two experimental approaches were used. First, incubated pro-oestrous pituitaries from hFSH-injected cycling and oestrogen-treated ovariectomized (OVX) rats were used to analyze the effect of calyculin, an inhibitor of intracellular phosphatases, on PR-dependent LH release, which was measured in the incubation medium by RIA. Second, pituitaries taken from hFSH-injected intact cycling and OVX rats and later incubated with P or GNRH1 were used to assess the phosphorylation rate of gonadotrope. The latter was analysed in formalin-fixed, paraffin-embedded tissue sections by immunohistochemistry using a MAB that recognizes the phosphorylated (p) form of PR at Ser294. Calyculin reduced the ovary-mediated inhibition of hFSH in GNRH1-stimulated LH secretion. In addition, the immunohistochemical expression of pSer294 PR was significantly reduced after ovarian stimulation with hFSH in pituitaries from pro-oestrous rats incubated with P or GNRH1. Altogether, these results suggested that the ovarian-dependent inhibitory effect of FSH injection on the preovulatory LH secretion in the rat may involve an increase in dephosphorylation of PR.

Cholinergic inputs to the amygdala and the control of gonadotrophin release

1980 ◽  
Vol 93 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Flavio Piva ◽  
José Borrell ◽  
Patrizia Limonta ◽  
Gilberto Gavazzi ◽  
Luciano Martini
Keyword(s):  
Nicotinic Receptors ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Muscarinic Agonist ◽  
Time Intervals ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Secretion ◽  
Cholinomimetic Drugs

Abstract. Adult female rats castrated 4 weeks before were implanted bilaterally into the basomedial area of the amygdala with drugs known to mimic or to counteract the actions of acetylcholine. The animals were sacrificed at different time intervals after the implantation of the different compounds, and serum levels of LH and FSH were measured by radioimmunoasay. The data obtained indicate that the intra-amygdalar implantation of the muscarinic blocker atropine induces a significant increase of the release of LH without altering FSH secretion. The implantation of two cholinomimetic drugs, pilocarpine, an almost pure muscarinic agonist, and carbachol, which possesses both muscarinic and nicotinic properties, exerted an inhibitory effect only on LH release. On the contrary, the intra-amygdalar placement of the nicotinic blocker mecamylamine was followed by an increase of FSH with no changes in LH. These observations may suggest that cholinergic signals reaching the amygdala may be of some relevance in the mechanisms controlling gonadotrophin secretion. Muscarinic receptors seem to play an inhibitory role in the regulation of LH secretion, while nicotinic receptors seem to modulate in an inhibitory way FSH release.

Reanalysis of the rat proestrous LH surge by deconvolution analysis

1993 ◽  
Vol 265 (5) ◽  
pp. R1222-R1222
Author(s):  
J. D. Veldhuis ◽  
M. L. Johnson ◽  
R. V. Gallo
Keyword(s):  
Estrous Cycle ◽  
Reference List ◽  
Deconvolution Analysis ◽  
Lh Surge ◽  
Low Level ◽  
Lh Release ◽  
Lh Secretion

Pages R240–R245: J. D. Veldhuis, M. L. Johnson, and R. V. Gallo. “Reanalysis of the rat proestrous LH surge by deconvolution analysis.” Page R244: Reference 7 was inadvertently dropped from the reference list by the printer. It should read: 7. Gallo, R. V. Pulsatile LH release during periods of low level LH secretion in the rat estrous cycle. Biol. Reprod. 24: 771–777, 1981.

scholarly journals No Evidence That RFamide-Related Peptide 3 Directly Modulates LH Secretion in the Ewe

Endocrinology ◽  
2016 ◽  
Vol 157 (4) ◽  
pp. 1566-1575 ◽  
Author(s):  
C. Decourt ◽  
K. Anger ◽  
V. Robert ◽  
D. Lomet ◽  
J. Bartzen-Sprauer ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Estradiol Benzoate ◽  
Inhibitory Effect ◽  
Minor Role ◽  
Gonadotropin Secretion ◽  
Related Peptide ◽  
Lh Pulsatility ◽  
Lh Release ◽  
A Minor ◽  
Lh Secretion

Abstract The neuropeptide RFamide-related peptide 3 (RFRP-3) has been implicated in the control of gonadotropin secretion in both birds and mammals. However, in mammals, depending on species, sex and photoperiod, inhibitory, excitatory, or no effect of RFRP-3 on the plasma concentration of LH has been reported. In the ewe, treatment with RFRP-3 either reduced LH concentration or had no effect, and treatment with an RFRP-3 receptor antagonist (ie, RF9) resulted in increased concentration of plasma LH. To clarify these conflicting results in the present study, a set of experiments was performed in ewes. Multiple iv injections of RFRP-3 (6 × 50 μg) in ovariectomized ewes had no effect on plasma LH pulsatility. In intact ewes a bolus injection (500 μg) or an injection (250, 500, or 1000 μg) followed by a 4-hour perfusion (250, 500, or 1000 μg · h−1) of RFRP-3 had no effect on the LH pulse induced by kisspeptin (6.5 μg). In ovariectomized, estrogen-replaced ewes, the LH surge induced by estradiol benzoate was not modified by a 24-hour perfusion of RFRP-3 (500 μg h−1). Finally, although treatment with RF9 induced a robust release of LH, treatment with a more selective RFRP-3 receptor antagonist, GJ14, resulted in no evident increase of LH. In contrast to the inhibitory effect previously suggested, our data are more consistent with the concept that RFRP-3 has no direct effect on LH secretion in ewes and that RF9 effect on LH release is likely not RFRP-3 receptor mediated. Hence, RFRP-3 probably has a minor role on the control of LH secretion in the ewe.

scholarly journals Effects of non-steroidal gonadal factors on LH secretion in female common carp during the reproductive cycle

2008 ◽  
Vol 53 (No. 9) ◽  
pp. 398-403
Author(s):  
J. Chyb ◽  
T. Mikolajczyk ◽  
M. Sokolowska-Mikolajczyk ◽  
M. Socha ◽  
P. Szczerbik ◽  
...  
Keyword(s):  
Common Carp ◽  
Reproductive Cycle ◽  
Inhibitory Effect ◽  
Gonad Maturity ◽  
Lh Release ◽  
Gonadal Recrudescence ◽  
Lh Secretion

The aim of this study was to evaluate the effects of recombinant human inhibin A, recombinant human activin A and desteroidized ovarian extract on LH secretion <I>in vitro</I> and <I>in vivo</I> in female common carp during different stages of reproductive cycle. Inhibin stimulated spontaneous as well as GnRH-stimulated LH release <I>in vivo</I> in fish during gonadal recrudescence. This hormone did not have an influence on spontaneous LH secretion in the periovulatory period, but had a slightly inhibitory effect on GnRH-stimulated LH release in this stage of gonad maturity. Activin decreased spontaneous LH secretion during gonadal recrudescence and increased LH secretion before ovulation, having no effects on GnRH-stimulated LH release during both stages of gonad maturity. The desteroidized ovarian extract failed to modify spontaneous LH secretion, but decreased GnRH-stimulated LH release during recrudescence and especially before ovulation. It is to conclude that these data suggest the differential role of inhibin/activin as substances in the regulation of LH secretion in common carp females.

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