Electrical Stimulation of the Arcuate Nucleus in Ovariectomized Rats Inhibits Episodic Luteinizing Hormone (LH) Release but Excites LH Release After Estrogen Priming12

Endocrinology ◽  
1976 ◽  
Vol 99 (3) ◽  
pp. 659-668 ◽  
Author(s):  
ROBERT V. GALLO ◽  
ROBERT B. OSLAND
Keyword(s):  
Electrical Stimulation ◽  
Luteinizing Hormone ◽  
Arcuate Nucleus ◽  
Ovariectomized Rats ◽  
Lh Release ◽  
Stimulation Of

LESIONS OF THE SUPRACHIASMATIC NUCLEI AND THE SEROTONIN-DEPENDENT PHASIC RELEASE OF LUTEINIZING HORMONE IN THE RAT: EFFECTS ON DRINKING RHYTHMICITY AND ON THE CONSEQUENCES OF PREOPTIC AREA STIMULATION

1980 ◽  
Vol 84 (2) ◽  
pp. 231-236 ◽  
Author(s):  
C. W. COEN ◽  
P. C. B. MacKINNON
Keyword(s):  
Electrical Stimulation ◽  
Luteinizing Hormone ◽  
Preoptic Area ◽  
Ovariectomized Rats ◽  
Suprachiasmatic Nuclei ◽  
Lh Release ◽  
Radiofrequency Lesions ◽  
Pharmacological Manipulations ◽  
Stimulation Of ◽  
Phasic Release

Ovariectomized rats in which <7% of the suprachiasmatic nuclei had been spared by bilateral radiofrequency lesions were distinguishable from those with >40% of the nuclei by their consistent failure to show the oestrogen-induced daily surge of LH, either with or without pharmacological manipulations of serotonin (5-HT), and also by their loss of the normal rhythmicity of drinking. Minor damage to structures adjacent to the suprachiasmatic nuclei was similar in both groups. The identical facility with which electrical stimulation of the preoptic area induced LH release in the two groups of animals suggested that they were not characterized by different degrees of damage to the preopticotuberal pathway. These results are considered in relation to evidence indicating that the suprachiasmatic nuclei represent the densest concentration of 5-HT terminals in the forebrain and also the site of a mechanism involved in the generation of circadian rhythms.

LUTEINIZING HORMONE RELEASING FACTOR IN ULTRAFILTRATES OF BLOOD COLLECTED FROM THE PITUITARY STALK OF OVARIECTOMIZED RATS AND RATS SUBJECTED TO ELECTRICAL STIMULATION OF THE PREOPTIC AREA

1972 ◽  
Vol 54 (2) ◽  
pp. 227-237 ◽  
Author(s):  
H. G. BURGER ◽  
G. FINK ◽  
V. W. K. LEE
Keyword(s):  
Electrical Stimulation ◽  
Luteinizing Hormone ◽  
Preoptic Area ◽  
Male Rats ◽  
Pituitary Stalk ◽  
Ovariectomized Rats ◽  
Serum Lh ◽  
Pituitary Glands ◽  
The Brain ◽  
Stimulation Of

SUMMARY The presence of luteinizing hormone releasing factor (LH-RF) activity was investigated in pituitary stalk and systemic blood collected from rats ovariectomized at least 3 weeks previously, and in stalk blood from male rats in which electrodes had been implanted in the medial preoptic area of the brain. Most of the assayable luteinizing hormone (LH) present in the blood samples was eliminated by acid-ethanol extraction followed by ultrafiltration. The ultrafiltrates were injected into ovariectomized rats treated with oestrogen and progesterone, and increments in the concentration of LH in the sera of these animals, estimated by radioimmunoassay, were taken as an indication that the filtrate was able to release LH from the anterior pituitary gland. The ultrafiltrates of both the stalk and systemic plasma from the ovariectomized rats exhibited LH-RF activity as did the ultrafiltrates of blood collected from the pituitary stalk of the male rats during electrical stimulation of the preoptic area; stalk blood collected from these animals before the current was applied appeared to be inactive. The LH-RF activity of the ultrafiltrates of systemic and pituitary stalk plasma taken from ovariectomized rats was similar, and, therefore, the possibility is raised that the response of the pituitary glands in ovariectomized rats treated with oestrogen and progesterone is of an all or none type. The presence of appreciable quantities of LH-RF in the systemic plasma of ovariectomized rats may explain the discrepancy between bioassay and immunoassay estimates of LH in the plasma of these animals. The rapid increase in the concentration of serum LH and in the LH-RF activity of pituitary stalk plasma which followed stimulation of the preoptic area suggests that this region of the brain may be important in the control of the secretion of LH in the male as well as in the female animal.

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.

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