scholarly journals Paraventricular α1- and α2-Adrenergic Receptors Mediate Hindbrain Lipoprivation-induced Suppression of Luteinizing Hormone Pulses in Female Rats

2008 ◽  
Vol 54 (3) ◽  
pp. 198-202 ◽  
Author(s):  
Somchai SAJAPITAK ◽  
Yoshihisa UENOYAMA ◽  
Shunji YAMADA ◽  
Mika KINOSHITA ◽  
Kinuyo IWATA ◽  
...  
Endocrinology ◽  
2008 ◽  
Vol 149 (6) ◽  
pp. 3016-3024 ◽  
Author(s):  
Somchai Sajapitak ◽  
Kinuyo Iwata ◽  
Mohammad Shahab ◽  
Yoshihisa Uenoyama ◽  
Shunji Yamada ◽  
...  

2015 ◽  
Vol 61 (4) ◽  
pp. 351-359 ◽  
Author(s):  
Yoshihisa UENOYAMA ◽  
Akira TANAKA ◽  
Kenji TAKASE ◽  
Shunji YAMADA ◽  
Vutha PHENG ◽  
...  

1972 ◽  
Vol 50 (8) ◽  
pp. 768-773 ◽  
Author(s):  
E. A. Ibrahim ◽  
B. E. Howland

The concentration of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in serum and pituitary glands was studied in intact female rats and rats that were ovariectomized on day 0 of the experiment and then starved or fed for 2, 4, 7, or 9 days. Ovariectomy resulted in enhanced rates of synthesis and release of FSH and LH as indicated by the significant (P < 0.01) rises in the concentration of both hormones in the pituitary gland and serum.Starvation resulted in a decrease in body and pituitary weight. The concentration of FSH and LH in pituitary glands of starved rats was higher (P < 0.05) than that in fed rats on days 7 and 9. The concentration of FSH and LH in serum of starved rats was increased after ovariectomy but the levels on days 7 and 9 were lower than those of fed rats.These results suggest that the synthesis of FSH and LH was enhanced in both starved and fed rats following ovariectomy while the rate of release of both hormones was decreased at 7 and 9 days of starvation in comparison with rats fed ad libitum.


2017 ◽  
Author(s):  
Alexander J. Riordan ◽  
Ari W. Schaler ◽  
Jackson B. Fried ◽  
Tracie A. Paine ◽  
Janice E. Thornton

ABSTRACTThe cognitive symptoms of schizophrenia are poorly understood and difficult to treat. Estrogens may mitigate these symptoms via unknown mechanisms. To examine these mechanisms, we tested whether increasing estradiol (E) or decreasing luteinizing hormone (LH) could rescue declarative memory in a phencyclidine (PCP) model of schizophrenia. We then assessed whether changes in cortical or hippocampal GABA may underlie these effects. Female rats were ovariectomized and injected subchronically with PCP. To modulate E and LH, animals received hormone capsules or Antide injections. Short-term episodic memory was assessed using the novel object recognition task. Brain expression of GAD67 was analyzed via western blot, and parvalbumin-containing cells were counted using immunohistochemistry. Some rats received hippocampal infusions of a GABAA agonist, GABAA antagonist, or GAD inhibitor before behavioral testing. We found that PCP reduced hippocampal GAD67 and abolished object recognition. Antide restored hippocampal GAD67 and rescued recognition memory in PCP-treated animals. Estradiol reversed PCP’s amnesic effect but failed to restore hippocampal GAD67. PCP did not cause significant differences in number of parvalbumin-expressing cells or cortical expression of GAD67. Hippocampal infusions of a GABAA agonist restored memory in PCP-treated rats. Blocking hippocampal GAD or GABAA receptors in ovx animals reproduced memory loss similar to PCP and inhibited estradiol’s memory rescue in PCP-treated animals. In summary, decreasing LH or increasing E can reverse memory loss in a PCP model of schizophrenia. Alterations in hippocampal GABA may contribute to both PCP’s effects on declarative memory and the hormones’ ability to reverse them.


2017 ◽  
Vol 233 (3) ◽  
pp. 281-292 ◽  
Author(s):  
Kinuyo Iwata ◽  
Yuyu Kunimura ◽  
Keisuke Matsumoto ◽  
Hitoshi Ozawa

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.


1991 ◽  
Vol 54 (3) ◽  
pp. 192-195 ◽  
Author(s):  
Lorenz Fehm ◽  
Jens Clausing ◽  
Werner Kern ◽  
Reinhard Pietrowsky ◽  
Jan Born

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