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 Regulation of Luteinizing Hormone and Catecholamine Release

1984 ◽  
Author(s):  
◽  
Benjamin Adler
Keyword(s):  
Median Eminence ◽  
Positive Feedback ◽  
Ovarian Hormones ◽  
Ovariectomized Rats ◽  
Ovarian Hormone ◽  
Synthesis Inhibitor ◽  
Feedback Effects ◽  
Lh Surge ◽  
Lh Release ◽  
Lh Secretion

These studies tested the interrelated hypotheses that the ovarian hormones produce their positive feedback effects on luteinizing hormone (LH) secretion through activation of noradrenergic and adrenergic systems in specific hypothalamic regions. Furthermore, the ovarian hormones may alter the activity of opioid neuropeptide and Gamma-Aminobutyric Acid (GABA) systems to produce these alterations in catecholamine transmission and gonadotropin secretion. Radioimmunoassays were utilized to determine plasma LH and median eminence LHRH, and hypothalamic catecholamine concentrations were measured by radioenzymatic assay. The first two studies tested whether epinephrine (EPI) synthesis inhibition blocks the accumulation of median eminence LHRH that precedes the ovarian hormone-induced LH surge and also to test whether the stimulatory ovarian hormone regimen enhances the activity of hypothalamic EPI systems. Ovariectomized rats were primed with estradiol (EB), followed 2 days later by progesterone (Prog.). Animals were treated before Prog, administration with saline, one of the EPI synthesis inhibitors SKF 64139 or LY 78335, or the norepinephrine (NE) synthesis inhibitor, FLA-63. The catecholamine synthesis inhibitors blocked or delayed the LH surge. FLA-63 completely prevented the accumulation of LHRH in the median eminence that preceded the rise in LH release. However, selective reduction in EPI levels with SKF 64139 only partially prevented this increase in LHRH. A second EPI synthesis inhibitor, LY 78335, delayed both the LH surge and the rise in LHRH. In a second experiment, the administration of EB plus Prog, to ovariectomized rats increased the alpha-methyltyrosine (aMT) induced depletion of EPI in the medial basal hypothalamus (MBH). The depletion of NE after synthesis inhibition was enhanced in both the MBH and preoptic-anterior hypothalamus (POA). Experiments 3 and 4 examined a possible mechanism underlying these ovarian hormone effects on LH release and catecholamine activity. These studies tested whether the opiate antagonist, naloxone, which increases LH release, enhances the activity of NE and EPI neurons in the hypothalamus, and also tested whether morphine, an opiate agonist which decreases LH release, depresses the activity of hypothalamic NE and EPI activity. Administration of naloxone to EB-primed rats increased LH release and potentiated the depletion of NE in the POA and MBH, and enhanced the decline of EPI and dopamine (DA) in the MBH, suggesting increased catecholamine activity in these regions. Administration of the opiate agonist, morphine, to rats pretreated with EB and Prog., decreased LH and decreased the depletion of the catecholamines in the POA and MBH, suggesting reduced activity. In most cases, naloxone antagonized the inhibitory effect of morphine. Experiments 3, 6, and 7 examined the involvement of (GABA) systems in the positive feedback effects of EB and Prog, on LHRH and LH release. These studies tested 1) the effects of GABAergic drugs on the LH surge induced by EB and Prog., 2) whether GABA agonists reduce NE and EPI activity in the hypothalamus, and 3) whether a GABA agonist prevents the accumulation of median eminence LHRH induced by EB and Prog. Ovariectomized rats received the stimulatory EB plus Prog, treatment. Simultaneously with Prog., rats received either saline, the barbiturate, phenobarbital, the GABAg agonist, baclofen, the GABA^ agonist, muscimol, or either the GABA^ antagonist, bicuculline, or the putative GABAg antagonist, 5-aminovalerate. Additional experiments tested the effects of the GABA drugs on LH release in ovariectomized, hormonally untreated rats and in response to exogenous LHRH. The LH surge induced by EB+Prog. was blocked by treatment with either baclofen, muscimol, or phenobarbital. Bicuculline was ineffective in preventing the effect of baclofen and phonobarbital but partially prevented the effect of muscimol. Neither baclofen nor muscimol significantly affected LH release in hormonally untreated, ovariectomized rats or in rats receiving LHRH administration. In the results of Experiment 6, in EB plus Prog.-treated rats, baclofen and muscimol significantly reduced the concentrations of EPI and NE in the POA and MBH and prevented their decline after administration of otMT, suggesting decreased catecholamine transmission. In Experiment 7, rats were primed with the ovarian hormones and received, concurrently with Prog., either saline, or baclofen. The GABAg agonist, baclofen, blocked the LH surge and selectively increased LHRH concentrations. Experiment 8 tested 1) whether baclofen reverses the enhancement of LH release and catecholamine activity produced by naloxone, and 2) whether the opiate antagonist, nalmefene, prevents the blockade of the LH surge produced by baclofen. In the first study of Experiment 8, naloxone increased LH release and enhanced catecholamine activity in EB-primed rats. Baclofen was unable to reverse these effects. In the second study, baclofen administration to EB plus P treated rats blocked the LH surge and concomitant administration of nalmefene was unable to prevent this effect of baclofen. These results suggest that: 1) the ovarian hormones activate both NE and EPI systems to stimulate the early afternoon rise of LHRH in the median eminence and to induce the subsequent LH surge, 2) the ovarian hormones may produce their positive feedback effects on LH secretion by removing an inhibitory GABA or opioid neuropeptide influence on catecholamine transmission, allowing NE and EPI to stimulate LHRH, and subsequently, LH release, and 3) these modulatory actions of GABA and opiates may represent effects of two parallel, yet independent hypothalamic systems which regulate catecholamine neurotransmission and subsequently LH secretion.

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 medial preoptic nucleus as a site of the thermogenic and metabolic actions of melanotan II in male rats

2014 ◽  
Vol 307 (2) ◽  
pp. R158-R166 ◽  
Author(s):  
Boris Monge-Roffarello ◽  
Sebastien M. Labbe ◽  
Christophe Lenglos ◽  
Alexandre Caron ◽  
Damien Lanfray ◽  
...  
Keyword(s):  
Metabolic Effects ◽  
Male Rats ◽  
Hypothalamic Nucleus ◽  
Preoptic Nucleus ◽  
Iodothyronine Deiodinase ◽  
Interscapular Brown Adipose Tissue ◽  
Medial Preoptic Nucleus ◽  
Brown Adipose ◽  
A Site ◽  
Melanotan Ii

The present study was designed to investigate the role of the medial preoptic nucleus (MPO) as a site of the thermogenic and metabolic effects of the α-melanocyte-stimulating hormone analog melanotan II (MTII). We also assessed the involvement of the dorsomedial hypothalamic nucleus (DMH) by investigating the effects of the MPO infusion of MTII in rats with DMH lesions produced by kainic acid. Infusion of MTII in the MPO led to increases in interscapular brown adipose tissue (iBAT) temperature and iBAT uptake of 14C-bromopalmitate. Both increases were blocked by DMH lesions. iBAT temperature increase (area under curve) and 14C-bromopalmitate uptake emerged as two correlated variables ( r = 0.63, P < 0.001). DMH lesions also blocked MTII-induced expression of mRNAs coding for proteins involved in 1) thermogenesis [type II iodothyronine deiodinase ( Dio2) and peroxisome proliferator-activated receptor gamma coactivator 1-α ( Pgc1α)], 2) lipolysis [hormone-sensitive lipase ( Hsl)], and 3) lipogenesis [diacylglycerol-O-acyltransferase 2 ( Dgat2), fatty acid synthase ( Fas)], in iBAT of rats killed 1 h after MPO infusion of MTII. MTII also stimulated expression of genes in iWAT but only in rats with DMH lesions. These genes included glucose transporter member 4 ( Glut4), glycerol-3-phosphate acyltransferase 3 ( Gpat3), Dgat1, Dgat2, triglyceride lipase ( Atgl), Hsl, and carnitine palmitoyltransferase 1β ( Cpt1β). Altogether, the present results reveal the MPO as a site of the thermogenic and metabolic actions of MTII. They also contribute to establish the MPO-DMH duet as a significant target for melanocortins to modulate energy homeostasis.

Comparison of the LH secretion patterns in the male rat following infusion of LRH and of the LRH-analogue buserelin®. Influence of castration and oestradiol benzoate on the efficiency of LH release

1983 ◽  
Vol 102 (2) ◽  
pp. 196-204 ◽  
Author(s):  
G. A. Schuiling ◽  
N. Pols-Valkhof ◽  
T. R. Koiter
Keyword(s):  
Area Under The Curve ◽  
Male Rats ◽  
Male Rat ◽  
Potency Ratio ◽  
Maximal Height ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Buserelin Treatment ◽  
Pre Treatment ◽  
Lh Secretion

Abstract. The LH releasing activities of LRH and the LRH-analogue buserelin® (HOE 766; (D-Ser (But)6-LRH(1–9)nona peptide-ethylamide) were compared in intact and short- and long-term castrated male rats, pre-treated (either 1 or 3 days) with oestradiol benzoate (EB) or oil. LRH and buserelin were infused iv at the constant rate of 104 ng/h for 21 h. Blood samples were taken from an intracarotid cannula. LH responses were judged on the basis of the mean maximal height of the LH concentration (MH; ng LH/ml plasma) and a parameter of total LH release, i.e. the area under the curve of LH concentrations plotted against time ('area under the curve', AUC; expressed in 'area units'). The release efficiency of LRH and buserelin, E (see for a definition: Materials and Methods), which informs on the total quantity of LH released in relation to pituitary LH content, was calculated by dividing the AUC × 100 by the pituitary LH content at the beginning of stimulation. Maximal plasma LH concentrations were observed between t= 1.5 and t=3 h after LRH and between t= 1.5 and t=9 after buserelin treatment. Both with LRH and buserelin the rise of LH secretion was greater the longer the animals were castrated and/or pre-treated with EB. The buserelin-induced LH response (with the exception of the responses induced in the EB-pre-treated, 4-weeks castrated rat) were about 2–2.5 times higher (MH) and larger (AUC) than the corresponding LRH-induced responses. The buserelin/LRH potency ratio, therefore, is about 2–2.5. EB-pre-treatment did not change the pituitary LH content. It therefore enhanced the efficiency of release of LH of both LRH and buserelin. Castration, on the other hand, caused an increase of the pituitary LH content: after 4 weeks it was raised by a factor 4. Since, however, the LH responses induced by LRH and buserelin were proportionally higher and larger, castration did not significantly change the efficiency of LH release. The results indicate that the efficiency of LH release can be changed by changes in the endocrine environment in the experimental animals, whilst for the magnitude of LH responses the pituitary LH content is also important. It is therefore suggested that the responsiveness of the pituitary gland to LRH (and agonistic analogues) is determined by (1) the state of the LH secretion mechanism and (2) the pituitary LH content.

EFFECTS OF NALOXONE ON LUTEINIZING HORMONE AND PROLACTIN IN SERUM OF RATS

1980 ◽  
Vol 85 (2) ◽  
pp. 307-315 ◽  
Author(s):  
M. S. BLANK ◽  
A. E. PANERAI ◽  
H. G. FRIESEN
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Immature Female ◽  
Subcutaneous Injections ◽  
Serum Lh ◽  
Opiate Peptides ◽  
Lh Release ◽  
Lh Secretion

The effects of subcutaneous injections of the opiate antagonist naloxone on the tonic and phasic secretion of prolactin and LH were studied in rats. During development, resting levels of prolactin in serum were decreased by naloxone (2·5 mg/kg body wt) on days 24,45 and 50 in female rats and on days 28,45 and 50 in male rats. In the adult, naloxone (2·5 mg/kg body wt) decreased basal levels of serum prolactin in male rats and levels during oestrus in female rats. In 25-day-old female rats, serum LH rose from resting levels within 7·5 min of naloxone administration (2·5 mg/kg body wt) and returned to pretreatment levels by 30 min, while prolactin fell by 7·5 min and remained low for as long as 60 min after treatment. Furthermore, a tenfold lower dose of naloxone (0·25 mg/kg body wt) did not raise basal levels of serum LH but still decreased resting levels of serum prolactin in immature female rats (24 days old). The effect of naloxone (2·5 mg/kg body wt) on phasic LH release was studied in 29-day-old immature female rats primed on day 27 with pregnant mare serum gonadotrophin (PMSG). In these PMSG-treated rats the onset of the prolactin surge was blunted by naloxone while it had no effect on phasic LH release. Naloxone (5 mg/kg body wt) also induced a rise in levels of serum LH in ovariectomized rats and, if administered with morphine, it reversed the short-term inhibition of LH secretion caused by morphine. However, naloxone was ineffective after pretreatment with oestradiol benzoate. These findings suggest that the responses of serum LH and prolactin to naloxone were dissociated and that oestrogens and opiate peptides may have interacted to regulate secretion of LH.

Further evidence of the dual role of noradrenaline in regulation of thyrotrophin secretion in male rats

1981 ◽  
Vol 97 (2) ◽  
pp. 213-220 ◽  
Author(s):  
P. T. Männistö ◽  
J. Mattila ◽  
J. Tuomisto
Keyword(s):  
Median Eminence ◽  
Third Ventricle ◽  
Inhibitory Effect ◽  
Dual Role ◽  
Male Rats ◽  
Noradrenergic Neurons ◽  
Stimulatory Action ◽  
Cold Response ◽  
Medial Basal Hypothalamus ◽  
Tsh Secretion

Abstract. The dual role previously suggested for noradrenergic neurons in TRH-TSH regulation was studied in male rats. α-Methyl-p-tyrosine (αMPT) significantly decreased brain noradrenaline (NA) and dopamine (DA) levels 0.5–6 h after the injection. Maximum inhibition of TSH cold-response occurred at 4 h. One h after administration of l-dopa the brain DA (but not NA) level was considerably elevated. TSH cold-response was not significantly changed. The effects of αMPT and Ca-fusarate on the cold-induced TSH secretion were antagonized by neither dihydroxyphenylserine (DOPS; this drug restores NA stores) nor by l-dopa (which restores DA levels). DOPS even potentiated the depressive effect of αMPT and Ca-fusarate. When given into the third ventricle, NA did not modify basal TSH levels but decreased the cold-induced TSH secretion. When infused directly into the median eminence of the medial basal hypothalamus, NA reduced both basal and cold-induced TSH secretion. Pinealectomy decreased the TSH cold-response but NA seemed to retain its ability to inhibit TSH secretion. These results demonstrate that besides the possible stimulatory action on TSH secretion, noradrenergic neurons also have an inhibitory effect outside the blood-brain barrier, possibly in the median eminence.

scholarly journals Implication of D2-like dopaminergic receptors in the median eminence during the establishment of long-day inhibition of LH secretion in the ewe

1999 ◽  
Vol 163 (2) ◽  
pp. 243-254 ◽  
Author(s):  
F Bertrand ◽  
J Thiery ◽  
S Picard ◽  
B Malpaux
Keyword(s):  
Median Eminence ◽  
Critical Role ◽  
Pulse Frequency ◽  
Prolactin Secretion ◽  
Dopaminergic Receptors ◽  
Long Day ◽  
Agonist And Antagonist ◽  
Lh Release ◽  
Lh Secretion ◽  
Short Days

In ewes, photoperiod modulates LH release and dopaminergic terminals in the median eminence (ME) have a critical role in the establishment of long-day inhibition of LH secretion. This study was undertaken to determine the type of dopaminergic receptors, D1-like or D2-like, that mediate the action of dopamine on LH secretion at the ME level in this situation. This was assessed, in ovariectomized and estradiol-treated ewes, with the use of reverse microdialysis in the ME in three experiments: first, when LH secretion was stimulated by short days, by determining the response to three doses (0.01, 0.1 or 1 mg/ml) of a D1-like (SKF38393) and a D2-like (quinpirole) agonist; secondly, during early long-day inhibition of LH secretion, by determining the ability of SKF38393 and quinpirole (1 mg/ml) to mimic the inhibitory effects of dopamine, after a blockade of its synthesis with alpha-methyl-para-tyrosine (alphaMPT; 2 mg/ml); and thirdly, during early long-day inhibition of LH secretion, by determining the response to three doses (0.009, 0.09 or 0.9 mg/ml) of a D1-like (SCH23390) and a D2-like (sulpiride) antagonist. In none of the conditions was effect of the D1-like analogs on LH secretion found, compared with the control treatments. In contrast, the D2-like analogs caused changes in LH secretion. First, with short days, quinpirole in the highest dose significantly reduced mean LH concentration (P<0.05) and LH pulse frequency (P<0.01). Secondly, with long days, addition of quinpirole to alphaMPT caused a significant decrease in LH secretion relative to alphaMPT alone (P<0.05). Thirdly, with long days, sulpiride at the highest dose significantly increased mean LH concentration (during the first 3 h of treatment, P<0.05) and LH pulse frequency (P<0.05). Prolactin secretion was also determined in these experiments, and D2-like agonist and antagonist caused an inhibition and a stimulation of prolactin secretion, respectively. These results demonstrate that, in the ME, inhibitory action of dopamine on LH secretion, critical for the initiation of long-day-induced inhibition, is mediated by D2-like, not D1-like, dopaminergic receptors.

Tamoxifen does not block the inhibitory effect of testosterone on FSH release in rats

1987 ◽  
Vol 114 (1) ◽  
pp. 84-89
Author(s):  
P. Negri-Cesi ◽  
F. Celotti ◽  
R. C. Melcangi ◽  
M. Zanisi ◽  
M. Motta
Keyword(s):  
Adult Male ◽  
Testosterone Propionate ◽  
Day Treatment ◽  
Elevated Serum ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Concomitant Treatment ◽  
Lh Release ◽  
Series Of Experiments

Abstract. The aim of the present experiments was to analyze whether the inhibitory effect exerted by testosterone on FSH release might be mediated by the intracerebral transformation of the hormone into oestrogenic metabolites. Advantage has been taken of the availability of the potent antioestrogen tamoxifen. Two series of experiments have been performed. In the first one, adult male rats have been castrated and submitted, beginning immediately after surgery, to a 6-day treatment with testosterone propionate (2 mg/rat/day), tamoxifen (50 or 200 μg/rat/day) or testosterone propionate (2 mg/rat/day) plus tamoxifen (either 50 or 200 μg/rat/day). In the second experiment, adult male rats have been castrated and submitted to the same 6-day treatments, beginning 4 weeks following orchidectomy. In both experiments, the animals were killed 24 h after the last injection, and serum levels of FSH and LH have been measured by radioimmunoassays. The results have clearly shown that, in both experiments, the administration of testosterone results in a significant decrease of serum FSH and in a total suppression of LH release. The administration of tamoxifen, in either dose, does not modify the elevated serum FSH and LH levels present in the orchidetomized animals, and does not antagonize the inhibitory effect on FSH and LH secretion exerted by the concomitant treatment with testosterone propionate. It is concluded that testosterone inhibits FSH secretion in orchidectomized rats acting as such, and not following aromatization to oestrogens.

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