Acute Elevations of Serum Luteinizing Hormone Induced by Kainic Acid, N-Methyl Aspartic Acid or Homocysteic Acid

1978 ◽  
Vol 26 (6) ◽  
pp. 352-358 ◽  
Author(s):  
M.T. Price ◽  
J.W. Olney ◽  
T.J. Cicero
1987 ◽  
Vol 241 (1) ◽  
pp. 309-311 ◽  
Author(s):  
M Sato ◽  
F Inoue ◽  
N Kanno ◽  
Y Sato

A novel ninhydrin-positive compound, N-methyl-D-aspartic acid, was identified in the muscle extracts of the blood shell, Scapharca broughtonii. This compound is already known to have potent neuroexcitatory activity, inducing hypermotility and strong releasing action of serum luteinizing hormone in mammals. This may be, however, the first finding of N-methyl-D-aspartic acid in natural products.


1975 ◽  
Vol 48 (3) ◽  
pp. 231-233
Author(s):  
P. Dandona ◽  
D. J. El Kabir ◽  
F. Naftolin ◽  
P. C. B. MacKinnon

1. The effect of long-acting thyroid stimulator (LATS) on the serum luteinizing hormone (LH) levels of the rat in pro-oestrus has been studied. 2. The injection of three out of four LATS-containing immunoglobulin G fractions caused an increase in amounts of serum LH. 3. Adrenalectomy and dexamethasone suppression did not alter this response. 4. Injection of large doses of adrenocorticotrophic hormone did not produce any increase in serum concentrations of LH. 5. It is postulated that LATS may have a direct effect on the release of LH from the pituitary gland.


1979 ◽  
Vol 91 (3) ◽  
pp. 591-600 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takenori Shioji Motoi Yasuda ◽  
Koji Koike ◽  
Keiichi Kurachi

ABSTRACT Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 μg of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin®) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (± se) serum prolactin (PRL) levels from 65.1 ± 23.0 to 10.4 ± 2.0 ng/ml, while LH (12.6 ± 2.1 to 24.8 ± 5.9 mIU/ml) and oestradiol (40.1 ± 7.6 to 111.4 ± 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after the injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.


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