EVIDENCE FOR A DOPAMINERGIC COMPONENT IN THE SERIES OF NEURAL EVENTS THAT LEAD TO THE PRO-OESTROUS SURGE OF LH

1977 ◽  
Vol 85 (1) ◽  
pp. 18-24 ◽  
Author(s):  
James A. Clemens ◽  
Frank C. Tinsley ◽  
Ray W. Fuller
Keyword(s):  
Luteinizing Hormone ◽  
Inhibitory Effects ◽  
Brain Dopamine ◽  
Lh Surge ◽  
Lh Release

ABSTRACT The possible participation of dopamine in the neural events that lead to the pro-oestrous surge of luteinizing hormone (LH) was investigated utilizing a dopaminergic ergoline derivative (lergotrile mesylate). Administration of reserpine (2.0 mg/kg, ip) to rats on the day of pro-oestrus depicted brain dopamine and norepinephrine and prevented the LH surge and ovulation. Administration of lergotrile mesylate prior to or at the same time as reserpine prevented the inhibitory effects of reserpine on LH release and on ovulation in about half of the animals. When lergotrile mesylate was given on the morning of pro-oestrus, the LH surge was advanced. The results indicate that there is a dopaminergic component in the series of neural events that precede the surge of LH on prooestrus, and that the dopaminergic stimulus precedes the LH surge by about 4–5 h.

scholarly journals Effect of androgen on Kiss1 expression and luteinizing hormone release in female rats

2017 ◽  
Vol 233 (3) ◽  
pp. 281-292 ◽  
Author(s):  
Kinuyo Iwata ◽  
Yuyu Kunimura ◽  
Keisuke Matsumoto ◽  
Hitoshi Ozawa
Keyword(s):  
Luteinizing Hormone ◽  
Arcuate Nucleus ◽  
Female Rats ◽  
Hormone Release ◽  
Lh Surge ◽  
Continuous Release ◽  
Ovulatory Dysfunction ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Hyperandrogenic women have various grades of ovulatory dysfunction, which lead to infertility. The purpose of this study was to determine whether chronic exposure to androgen affects the expression of kisspeptin (ovulation and follicle development regulator) or release of luteinizing hormone (LH) in female rats. Weaned females were subcutaneously implanted with 90-day continuous-release pellets of 5α-dihydrotestosterone (DHT) and studied after 10 weeks of age. Number of Kiss1-expressing cells in both the anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC) was significantly decreased in ovary-intact DHT rats. Further, an estradiol-induced LH surge was not detected in DHT rats, even though significant differences were not observed between DHT and non-DHT rats with regard to number of AVPV Kiss1-expressing cells or gonadotrophin-releasing hormone (GnRH)-immunoreactive (ir) cells in the presence of high estradiol. Kiss1-expressing and neurokinin B-ir cells were significantly decreased in the ARC of ovariectomized (OVX) DHT rats compared with OVX non-DHT rats; pulsatile LH secretion was also suppressed in these animals. Central injection of kisspeptin-10 or intravenous injection of a GnRH agonist did not affect the LH release in DHT rats. Notably, ARC Kiss1-expressing cells expressed androgen receptors (ARs) in female rats, whereas only a few Kiss1-expressing cells expressed ARs in the AVPV. Collectively, our results suggest excessive androgen suppresses LH surge and pulsatile LH secretion by inhibiting kisspeptin expression in the ARC and disruption at the pituitary level, whereas AVPV kisspeptin neurons appear to be directly unaffected by androgen. Hence, hyperandrogenemia may adversely affect ARC kisspeptin neurons, resulting in anovulation and menstrual irregularities.

Evidence for the involvement of central catecholaminergic mechanisms in mediating the preovulatory surge of luteinizing hormone in the domestic hen

1982 ◽  
Vol 94 (2) ◽  
pp. 295-304 ◽  
Author(s):  
P. G. Knight ◽  
S. C. Wilson ◽  
R. T. Gladwell ◽  
F. J. Cunningham
Keyword(s):  
Steady State ◽  
Luteinizing Hormone ◽  
Pharmacological Treatments ◽  
Ovulatory Cycle ◽  
Lh Surge ◽  
Dopaminergic Mechanisms ◽  
Lh Release ◽  
Noradrenaline And Adrenaline ◽  
Domestic Hen ◽  
Catecholaminergic Mechanisms

The effects of various pharmacological treatments, designed to perturb central catecholaminergic neurotransmission, on the pattern of LH release during the preovulatory period in the domestic hen were studied. Treatment of hens with either l-dihydroxyphenylalanine or diethyldithiocarbamate which raised the concentration of dopamine in the hypothalamus by 42 and 110% respectively, or with apomorphine, attenuated the preovulatory surge of LH. In contrast, treatment with either α-methyl-p-tyrosine which produced a 65% decline in the concentration of dopamine in the hypothalamus without affecting the concentrations of noradrenaline or adrenaline or treatment with pimozide did not affect the LH surge. While treatment with propranolol was similarly ineffective, phenoxybenzamine attenuated the LH surge to a marked extent. These observations suggest that the preovulatory surge of LH in the hen is influenced by facilitatory α-adrenergic and inhibitory dopaminergic mechanisms. Evidence to corroborate these findings was sought by determining the steady-state concentrations of dopamine, noradrenaline and adrenaline in five discrete diencephalic regions of the hen throughout the ovulatory cycle.

Pulsatile Luteinizing Hormone (LH) Release during the Progesterone-Induced LH Surge in the Female Rhesus Monkey*

Endocrinology ◽  
1987 ◽  
Vol 120 (6) ◽  
pp. 2265-2271 ◽  
Author(s):  
E. TERASAWA ◽  
C. KROOK ◽  
S. EMAN ◽  
G. WATANABE ◽  
W. E. BRIDSON ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Rhesus Monkey ◽  
Lh Surge ◽  
Female Rhesus ◽  
Lh Release ◽  
Female Rhesus Monkey

scholarly journals Optogenetic Activation of Arcuate Kisspeptin Neurons Generates a Luteinizing Hormone Surge-Like Secretion in an Estradiol-Dependent Manner

2021 ◽  
Vol 12 ◽  
Author(s):  
Xian-Hua Lin ◽  
Geffen Lass ◽  
Ling-Si Kong ◽  
Hui Wang ◽  
Xiao-Feng Li ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Brain Area ◽  
Estradiol Benzoate ◽  
Dependent Manner ◽  
Lh Surge ◽  
Expected Time ◽  
17Β Estradiol ◽  
Stimulation Period ◽  
Lh Release ◽  
Lh Secretion

Traditionally, the anteroventral periventricular (AVPV) nucleus has been the brain area associated with luteinizing hormone (LH) surge secretion in rodents. However, the role of the other population of hypothalamic kisspeptin neurons, in the arcuate nucleus (ARC), has been less well characterized with respect to surge generation. Previous experiments have demonstrated ARC kisspeptin knockdown reduced the amplitude of LH surges, indicating that they have a role in surge amplification. The present study used an optogenetic approach to selectively stimulate ARC kisspeptin neurons and examine the effect on LH surges in mice with different hormonal administrations. LH level was monitored from 13:00 to 21:00 h, at 30-minute intervals. Intact Kiss-Cre female mice showed increased LH secretion during the stimulation period in addition to displaying a spontaneous LH surge around the time of lights off. In ovariectomized Kiss-Cre mice, optogenetic stimulation was followed by a surge-like secretion of LH immediately after the stimulation period. Ovariectomized Kiss-Cre mice with a low dose of 17β-estradiol (OVX+E) replacement displayed a surge-like increase in LH release during period of optic stimulation. No LH response to the optic stimulation was observed in OVX+E mice on the day of estradiol benzoate (EB) treatment (day 1). However, after administration of progesterone (day 2), all OVX+E+EB+P mice exhibited an LH surge during optic stimulation. A spontaneous LH surge also occurred in these mice at the expected time. Taken together, these results help to affirm the fact that ARC kisspeptin may have a novel amplificatory role in LH surge production, which is dependent on the gonadal steroid milieu.

Evidence for a stimulatory β-adrenergic component in the release of the ovulatory LH surge in pro-oestrous rats

1985 ◽  
Vol 106 (2) ◽  
pp. 143-151 ◽  
Author(s):  
M. H. Al-Hamood ◽  
D. P. Gilmore ◽  
C. A. Wilson
Keyword(s):  
Adrenergic Receptor ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Adrenergic System ◽  
Receptor Subtypes ◽  
Inhibitory Effects ◽  
Pharmacological Agents ◽  
Lh Surge ◽  
Pentobarbitone Sodium ◽  
Lh Release

ABSTRACT The effect on ovulation of intraventricular infusions of noradrenaline, adrenaline and various pharmacological agents acting on the adrenergic receptor subtypes were investigated in cyclic female rats on the day of pro-oestrus. The inhibitory effects on ovulation of the different infusions were monitored by administering the drugs before 11.00 h (several hours before the critical period for the ovulatory LH surge). In experiments designed to show how the drugs under investigation might stimulate ovulation, pentobarbitone sodium (35 mg/kg) was given at 14.30 h; this anaesthetic inhibits ovulation and its effects can be overcome by substances that advance the preovulatory LH surge. Noradrenaline (an α-agonist) stimulated ovulation when administered on the morning of pro-oestrus to rats injected with pentobarbitone early in the afternoon of the same day. Phenoxybenzamine and phentolamine (non-selective α-antagonists) and clonidine (a selective α2-agonist) all inhibited ovulation when infused on the morning of pro-oestrus. Yohimbine (a moderately selective α2-antagonist) neither stimulated nor inhibited ovulation. Both isoprenaline (a non-selective β-agonist) and fenoterol (a selective β2-agonist) stimulated ovulation in pentobarbitone-treated rats when administered on the morning of pro-oestrus and fenoterol was also able to overcome the pentobarbitone block when infused later in the afternoon. Propranolol (a non-selective β-antagonist) and metoprolol (a selective β1-antagonist) were stimulatory only when administered in the afternoon. Adrenaline (both an α- and β-agonist), prenalterol (a selective β1-agonist), atenolol (a selective β1-antagonist) and ICI 118, 551 (a selective β2-antagonist) neither stimulated nor inhibited ovulation. The effect of intraventricular infusions of two selected β-adrenergic drugs was also investigated in ovariectomized rats primed with 2 μg oestradiol benzoate 48 h previously. Isoprenaline and fenoterol were able to stimulate LH release at 40 and 10 min respectively after their administration. These results suggest a possible involvement of a stimulatory β2-adrenergic component in the neural regulation of the preovulatory LH surge along with the well-documented α-stimulatory component, which together may mask the possible inhibitory effects of a β1-adrenergic system. J. Endocr. (1985) 106, 143–151

scholarly journals Differential Expression of Estrogen Receptors in the Hypothalamus Underlies the Bimodal Effects of Estradiol on Luteinizing Hormone Release

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A536-A537
Author(s):  
Patricia Costa Henriques ◽  
Nayara Soares Sena Aquino ◽  
Roberta Araújo-Lopes ◽  
Juneo Freitas Silva ◽  
Candido Celso Coimbra ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Estrogen Receptors ◽  
Negative Feedback ◽  
Feedback Effects ◽  
Lh Surge ◽  
Neuronal Populations ◽  
17Β Estradiol ◽  
Lh Release ◽  
Positive And Negative Feedback

Abstract Low 17β-estradiol (E2) levels suppress luteinizing hormone (LH) release, while high E2 stimulates an LH surge in the positive-feedback required for ovulation. Kisspeptin (Kp) neurons in the anteroventral periventricular (AVPV) and arcuate (ARC) nuclei of hypothalamus have been implicated in E2 positive- and negative-feedback effects, respectively. However, how E2 differentially regulates these two neuronal populations remains unknown. We investigated whether neurons in the AVPV and ARC are differently responsive to changes in E2 levels and the regulatory role of estrogen receptors (ERs). Ovariectomized (OV) rats received oil or E2 at doses of 4 (OVE-4), 40 (OVE-40), or 80 (OVE-80) µg/kg. Rats on diestrus (DI) and proestrus (PRO) were used as physiological controls. OV rats were also treated with 0.02, 0.2 or 2.0 mg/kg of propyl pyrazole triol (PPT), or 6 mg/kg of diarylpropionitrile (DPN). Serial blood samples were collected for hormonal measurements. Brains were processed for immunohistochemistry and qPCR analyses in the AVPV and ARC. The E2 doses gradually increased plasma E2, with PRO levels being attained in OVE-80 rats. OVE-80 rats displayed a PRO-like LH surge, while LH levels were constantly suppressed in OVE-4 rats. Progesterone receptor (PR) was used as an index of E2 responsiveness. PR expression was increased in the AVPV of PRO and OVE-80 rats, associated with c-Fos expression and occurrence of LH surge. In the ARC, both low and high E2 induced PR expression and reduced the number of Kp-immunoreactive (ir) neurons, consistent with the negative feedback effects on LH. E2 at 4 or 80 µg/kg equally induced PR expression in 90% of ARC Kp-ir neurons. Despite the higher sensitivity to E2 in the ARC, the percentage of neurons expressing ERα was lower in the ARC compared with AVPV. However, Esr1 expression was 2-fold higher in the ARC than in AVPV for low E2 levels, whereas both Esr1 and Esr2 were more expressed in the AVPV under high E2 status. Notably, Esr1/Esr2 ratio was twice as high in the ARC as in the AVPV regardless of E2 levels, suggesting a stronger ERβ inhibition over ERα in the AVPV. Accordingly, ERα selective activation with PPT increased PR in the ARC at the doses of 0.2 and 2.0 mg/kg, reducing plasma LH, while only the highest dose was able to stimulate PR expression in the AVPV. ERβ activation with DPN, in turn, had no effect in OV rats but amplified the induction of AVPV PR and the size of the LH surge in OVE-80 rats. Thus, we provide evidence that ARC and AVPV neurons are responsive to low and high E2 levels, respectively. ARC is 10 times more sensitive to ERα activation than AVPV, whereas ERβ positively modulates AVPV responsiveness to high E2. These differential responses to E2 seem to be related to differences in the relative Esr1 and Esr2 expression in the ARC and AVPV. Our findings suggest that hypothalamic differences in the relative expression of ERs play a key role in the bimodal regulation of LH release by E2.

Androgenic and oestrogenic steroid participation in feedback control of luteinizing hormone secretion in male sheep

1983 ◽  
Vol 102 (4) ◽  
pp. 499-504 ◽  
Author(s):  
M. J. D'Occhio ◽  
B. D. Schanbacher ◽  
J. E. Kinder
Keyword(s):  
Luteinizing Hormone ◽  
Pulse Generator ◽  
Hormone Secretion ◽  
Pulse Interval ◽  
Serum Concentrations ◽  
Luteinizing Hormone Secretion ◽  
Lh Release ◽  
Lh Secretion ◽  
Additional Feedback ◽  
Male Sheep

Abstract. The acute castrate ram (wether) was used as an experimental model to investigate the site(s) of feedback on luteinizing hormone (LH) by testosterone, dihydrotestosterone and oestradiol. At the time of castration, wethers were implanted subdermally with Silastic capsules containing either crystalline testosterone (three 30 cm capsules), dihydrotestosterone (five 30 cm capsules) or oestradiol (one 6.5 cm capsule). Blood samples were taken at 10 min intervals for 6 h 2 weeks after implantation to determine serum steroid concentrations and to characterize the patterns of LH secretion. Pituitary LH response to exogenous LRH (5 ng/kg body weight) were also determined at the same time. The steroid implants produced serum concentrations of the respective hormones which were either one-third (testosterone) or two-to-four times (dihydrotestosterone, oestradiol) the levels measured in rams at the time of castration. Non-implanted wethers showed rhythmic pulses of LH (pulse interval 40–60 min) and had elevated LH levels (16.1 ± 1.6 ng/ml; mean ± se) 2 weeks after castration. All three steroids suppressed pulsatile LH release and reduced mean LH levels (to below 3 ng/ml) and pituitary LH responses to LRH. Inhibition of pulsatile LH secretion by all three steroids indicated that testosterone as well as its androgenic and oestrogenic metabolites can inhibit the LRH pulse generator in the hypothalamus. Additional feedback on the pituitary was indicated by the dampened LH responses to exogenous LRH.

Role of Ca2+ and Na+ on luteinizing hormone release from the calf pituitary

1988 ◽  
Vol 255 (4) ◽  
pp. E469-E474
Author(s):  
J. P. Kile ◽  
M. S. Amoss
Keyword(s):  
Luteinizing Hormone ◽  
Ionophore A23187 ◽  
Channel Blockers ◽  
Hormone Release ◽  
Primary Cells ◽  
Rat Pituitary ◽  
Voltage Dependent ◽  
Lh Release ◽  
Ca2 Channels

It has been proposed that gonadotropin-releasing hormone (GnRH) stimulates Ca2+ entry by activation of voltage-independent, receptor-mediated Ca2+ channels in the rat gonadotroph. Little work has been done on the role of calcium in GnRH-induced luteinizing hormone (LH) release in species other than the rat. Therefore, this study was done to compare the effects of agents that alter Ca2+ or Na+ entry on LH release from calf anterior pituitary primary cells in culture. GnRH (100 ng/ml), Ca2+ ionophore A23187 (2.5 microM), and the depolarizing agent ouabain (0.1-10 microM) all produced significant increases (P less than 0.05) in LH release; these effects were significantly reduced when the cells were preincubated with the organic Ca2+ channel blockers nifedipine (1-10 microM) and verapamil (1-10 microM) and with Co2+ (0.01-1 mM). The effect of ouabain was inhibited by tetrodotoxin (TTX; 1-10 nM) as well as by nifedipine at 0.1-10 microM. In contrast to its effect on rat pituitary LH release, TTX significantly inhibited GnRH-stimulated LH release at 1-100 nM. These results suggest that GnRH-induced LH release may employ Ca2+ as a second messenger in bovine gonadotrophs and support recent speculation that GnRH-induced Ca2+ mobilization may in part be voltage dependent.

RELATIONSHIP BETWEEN BLOOD LEVELS OF LUTEINIZING HORMONE AND TESTOSTERONE IN BULLS, AND THE EFFECTS OF SEXUAL STIMULATION

1971 ◽  
Vol 50 (3) ◽  
pp. 457-466 ◽  
Author(s):  
C. B. KATONGOLE ◽  
F. NAFTOLIN ◽  
R. V. SHORT
Keyword(s):  
Luteinizing Hormone ◽  
Immediate Release ◽  
Blood Levels ◽  
Testosterone Levels ◽  
Peripheral Plasma ◽  
Sexual Stimulation ◽  
Maximal Stimulation ◽  
Cyclical Pattern ◽  
Lh Release ◽  
Competitive Protein Binding

SUMMARY Luteinizing hormone (LH) and testosterone were measured in the peripheral plasma of two bulls by radioimmunoassay and competitive protein binding techniques. Samples were collected from an indwelling jugular catheter once an hour for 24 h, and then at more frequent intervals after a number of experimental procedures. Each bull showed its own characteristic pattern of cyclic LH changes, with 5–10 peaks during 24 h that were apparently unrelated to daylight, feeding or sleep. Each LH peak was associated with a testosterone peak; the LH concentrations ranged from 5 to 50 ng/ml, and those of testosterone from 2 to 20 ng/ml. Sexual stimulation, such as the sight of a cow, or 'teasing', or on one occasion the act of ejaculation itself, caused an immediate release of a large amount of LH. If the testosterone levels were low at the time, the LH peak was followed by a testosterone peak. But when the testosterone levels were high at the time of LH discharge, the testis seemed to be unable to respond any further. An intravenous injection of 500 i.u. human chorionic gonadotrophin was associated with LH release and caused the testosterone levels to rise to maximal values of 22 ng/ml within 1½ h. It is concluded that the cyclical pattern of LH release is due to some inherent central rhythm, and that each transient LH peak results in transient maximal stimulation of testicular testosterone secretion.

EFFECT OF HYPOTHALAMIC DEAFFERENTATION ON THE CONTROL OF LUTEINIZING HORMONE SECRETION

1970 ◽  
Vol 46 (1) ◽  
pp. 1-7 ◽  
Author(s):  
S. TALEISNIK ◽  
M. E. VELASCO ◽  
J. J. ASTRADA
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Positive Feedback ◽  
Hormone Secretion ◽  
Feedback Effect ◽  
Luteinizing Hormone Secretion ◽  
Ovarian Steroids ◽  
Medial Hypothalamus ◽  
Lh Release ◽  
Positive Feedback Effect

SUMMARY The influence that the interruption of the neural afferents to the hypothalamus exerts on ovulation and on the release of luteinizing hormone (LH) was studied in the rat. Animals with retrochiasmatic sections interrupting the neural connexions between the medial hypothalamus and the preoptic area (POA) showed constant oestrus and failed to ovulate. Animals in which the dorsal neural afferents to the POA were transected had oestrous cycles and ovulated normally. The positive feedback effect of progesterone on LH release in spayed animals primed either with 20 μg. oestradiol benzoate or 2·5 mg. testosterone propionate 3 days before was studied. Transection of the dorsal afferents to the POA favoured an increase in plasma LH, but in animals with retrochiasmatic sections the response was abolished. However, the negative feedback effect of ovarian steroids operated after both types of transection because an increase in plasma LH occurred after ovariectomy. It is concluded that the negative feedback effect of ovarian steroids acts on the medial hypothalamus which can maintain a tonic release of gonadotrophins in the absence of steroids. In contrast, the POA involved in the positive feedback effect of progesterone is concerned with the phasic release of LH.

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