Evidence for an Inhibitory Dopaminergic and Stimulatory Noradrenergic Hypothalamic Influence of PMS-Induced Ovulation in the Immature Rat. I. Catecholamine Turnover Changes in Relation to the Critical Period

1977 ◽  
Vol 24 (5-6) ◽  
pp. 270-288 ◽  
Author(s):  
A. Löfström ◽  
L.F. Agnati ◽  
K. Fuxe
1986 ◽  
Vol 251 (3) ◽  
pp. E362-E365 ◽  
Author(s):  
L. L. Espey ◽  
D. H. Miller ◽  
H. S. Margolius

Ovarian kinin-generating capacity was determined during induced ovulation in immature Wistar rats. The onset of ovulation was monitored by counting the number of ova in the oviducts at 2-h intervals after the administration of human chorionic gonadotropin (hCG). Ova began to appear in significant numbers at 14 h after hCG, with an average of 7.6 +/- 2.3 ova/rat. By 16 h after hCG, the oviducts contained 32.7 +/- 4.1 ova/rat. The ovaries from each group of animals were homogenized in phosphate-buffered saline, and extracts of this tissue were incubated for 200 min to allow the generation of kinins from endogenous kininogen. The amount of kinin generated by this procedure was measured by radioimmunoassay. At 0 h (i.e., just before the administration of hCG), the ovaries contained 5.90 +/- 0.60 pg kinin/micrograms protein per 200 min in the ovarian extract. By 4 h after hCG, the kinins increased significantly (P less than 0.05) to 13.16 +/- 3.61 pg kinin/micrograms protein. The kinins progressively increased (P less than 0.001) to 67.88 +/- 23.26 pg kinin/micrograms protein by 16 h after hCG. Indomethacin and cycloheximide significantly inhibited both kinin-generating activity and ovulation. These data suggest that kinin-forming activity and kinins may have a role in the ovulatory process of mammals.


1965 ◽  
Vol 119 (2) ◽  
pp. 331-334 ◽  
Author(s):  
M. X. Zarrow ◽  
S. K. Sundaram ◽  
M. Stob

1975 ◽  
Vol 64 (2) ◽  
pp. 337-347 ◽  
Author(s):  
CATHERINE A. WILSON ◽  
C. E. HORTH ◽  
A. McNEILLY ◽  
P. G. McDONALD

SUMMARY Serotonin (50 and 100 mg/kg), given subcutaneously, inhibited induced ovulation in immature rats treated with pregnant mare serum gonadotrophin (PMSG). A single injection was effective if given 52–55 h after the PMSG, i.e. in the 3 h period after the critical period before ovulation. The injection of serotonin inhibited the release of luteinizing hormone (LH) from the pituitary since the pituitary levels were higher than in the control animals and there was complete inhibition of the plasma LH surge. The antiovulatory effect was reversed by administration of progesterone and endogenous plasma progesterone levels were reduced in the late evening after serotonin treatment. The site of action of serotonin appeared to be peripheral since it inhibited induced ovulation in hypophysectomized rats but was without effect in intact rats treated intraventricularly. It is suggested that progesterone is essential for the occurrence of induced ovulation and serotonin inhibits either its secretion at the ovarian level or its passage away from the ovary.


1979 ◽  
Vol 35 (5) ◽  
pp. 692-694 ◽  
Author(s):  
V. D. Parker ◽  
K. F. A. Soliman ◽  
C. A. Walker

Endocrinology ◽  
1969 ◽  
Vol 84 (5) ◽  
pp. 1274-1276 ◽  
Author(s):  
M. X. ZARROW ◽  
R. V. GALLO

Endocrinology ◽  
1964 ◽  
Vol 74 (3) ◽  
pp. 309-313 ◽  
Author(s):  
DAVID L. QUINN ◽  
M. X. ZARROW

1963 ◽  
Vol 26 (2) ◽  
pp. 181-188 ◽  
Author(s):  
M. X. ZARROW ◽  
D. L. QUINN

SUMMARY Superovulation can be induced in the immature rat by PMS alone or PMS followed by HCG. Treatment with PMS alone caused an initial average response of 2·8 ova at an age of 20 days and a maximum average response of 70·8 ova at age 28. Treatment with PMS and HCG resulted in an initial average response of 0·3 ova at age 18 days and an average maximum of 61 ova at 22 days of age. A marked drop to approximately 8–10 ova was noted at 45 days of age following both types of treatment. Hypophysectomy revealed that the pituitary gland was necessary for the release of ova following injection of PMS alone. Removal of the pituitary gland as late as 52 hr. after injection of PMS prevented ovulation. Inhibition of ovulation by treatment with dibenamine, SKF-501, atropine and 'Nembutal' following injection of PMS alone led to the concept that superovulation following PMS involves a neural link that is responsible for the endogenous release of LH.


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