Luteinizing Hormone-Releasing Hormone (LH-RH) Neurons in Cultures of Fetal Rat Hypothalamus

1979 ◽  
Vol 28 (2) ◽  
pp. 131-137 ◽  
Author(s):  
S.C. Feldman ◽  
A.B. Johnson ◽  
M.B. Bornstein ◽  
G.T. Campbell
Keyword(s):  
Luteinizing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Fetal Rat ◽  
Lh Rh

FURTHER STUDIES ON ENZYMIC INACTIVATION OF LUTEINIZING HORMONE – RELEASING HORMONE (LH-RH) BY PEPTIDASES IN THE RAT HYPOTHALAMUS

1975 ◽  
Vol 79 (1) ◽  
pp. 7-15 ◽  
Author(s):  
E. C. Griffiths ◽  
K. C. Hooper ◽  
C. R. N. Hopkinson
Keyword(s):  
Enzyme Activity ◽  
Luteinizing Hormone ◽  
Assay System ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Lh Rh ◽  
A Site

ABSTRACT Luteinizing hormone-releasing hormone (LH-RH) is known to be inactivated by peptidases in the rat hypothalamus with consequent loss of LH-releasing ability. To make a further study of the peptidases' action on the decapeptide, synthetic LH-RH and its [1–9NH2] analogue were incubated with the supernatant hypothalamic fraction containing the enzyme activity. Using an assay system measuring gonadotrophin release in ovariectomized/steroid-primed rats, both LH-RH and the [1–9NH2] analogue were found to be inactivated to different extents after incubation with the fraction, the analogue completely losing both LH- and FSH-releasing activity, and the releasing hormone almost completely losing its LH- and totally losing its FSH-releasing activity. The findings extend the initial studies by showing that the peptidases can remove both the decapeptide's intrinsic LH- and FSH-releasing activity and that these enzymes act on LH-RH at a site other than the C-terminal glycinamide, since they are able to inactivate the [1–9NH2] analogue lacking this residue.

THE PRESENCE OF PEPTIDASES IN THE RAT HYPOTHALAMUS INACTIVATING LUTEINIZING HORMONE RELEASING HORMONE (LH-RH)

1974 ◽  
Vol 77 (3) ◽  
pp. 435-442 ◽  
Author(s):  
E. C. Griffiths ◽  
K. C. Hooper ◽  
S. L. Jeffcoate ◽  
D. T. Holland
Keyword(s):  
Luteinizing Hormone ◽  
Reproductive Function ◽  
Assay Method ◽  
Supernatant Fraction ◽  
Peptidase Activity ◽  
Female Rat ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Lh Rh

ABSTRACT The presence of peptidases in the rat hypothalamus inactivating luteinizing hormone-releasing hormone (LH-RH) has previously been demonstrated using an indirect assay method. With the development of a sensitive and specific radioimmunoassay for the releasing hormone, this technique was employed in the study of the peptidases inactivating LH-RH. It was found that supernatant fractions from both male and female rat hypothalami rapidly inactivated LH-RH, and that the peptidase activity of the supernatant fraction was higher in male than in female animals though the particulate fraction's activity was about the same in both sexes. Peptidase activity was also considerably greater in the supernatant than in the particulate fraction. These results confirm that the hypothalamus contains peptidases capable of inactivating LH-RH and give a direct indication that the enzymes may be involved in the central nervous system's control of reproductive function.

EFFECT OF CORTISOL OR ADRENOCORTICOTROPHIN ON RELEASE OF LUTEINIZING HORMONE INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE IN THE DAIRY HEIFER

1982 ◽  
Vol 92 (1) ◽  
pp. 141-146 ◽  
Author(s):  
R. L. MATTERI ◽  
G. P. MOBERG
Keyword(s):  
Luteinizing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Dairy Heifers ◽  
Significant Difference ◽  
Significant Depression ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
And Control ◽  
Slight Depression

During treatment with cortisol or ACTH, dairy heifers were given two doses of LH releasing hormone (LH-RH) spaced 1·5 h apart. Serum concentrations of cortisol and LH were monitored during each treatment. Treatment with both ACTH and cortisol raised plasma cortisol levels above the respective saline controls (P<0·001). Neither treatment affected basal LH concentrations. A slight depression in LH response was seen in the cortisol-treated animals after the first LH-RH injection, as shown by a statistically significant depression at three of the sample times. There was no significant difference between treated and control LH values after the second LH-RH administration. Treatment with ACTH resulted in significantly reduced LH values at all sample times after both injections of LH-RH.

Melatonin inhibits luteinizing hormone releasing hormone (LHRH) induction of LH release from fetal rat pituitary cells

1995 ◽  
Vol 184 (2) ◽  
pp. 109-112 ◽  
Author(s):  
Atsuhiko Hattori ◽  
Damon C. Herbert ◽  
Mary K. Vaughan ◽  
Ken Yaga ◽  
Russel J. Reiter
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Cells ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Fetal Rat ◽  
Rat Pituitary ◽  
Lh Release ◽  
Rat Pituitary Cells

Acidic Aqueous Extraction of Hypothalamic Luteinizing Hormone Releasing Hormone to Study Biological Effects

1974 ◽  
Vol 52 (3) ◽  
pp. 754-758 ◽  
Author(s):  
S. H. Shin ◽  
C. J. Howitt
Keyword(s):  
Luteinizing Hormone ◽  
Biological Effects ◽  
Extraction Procedure ◽  
Extraction Methods ◽  
Water Soluble ◽  
Acid Extraction ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Aqueous Solvent ◽  
Lh Rh

Several aqueous solvent systems were tested for their efficiency in extracting luteinizing hormone releasing hormone (LH-RH) from rat hypothalamus. Although LH-RH is a water-soluble decapeptide, neutral distilled water extracted only 10% of the LH-RH obtained using acid extraction methods. The efficiency of the acid extraction procedure suggests that in the hypothalamus the releasing hormone is bound to a relatively large molecular weight compound. Using the acidic extraction procedure, we found that hypothalamic LH-RH content is significantly lower in the castrated animal than in the normal rat.

PROLONGED RELEASE BY DIOESTROUS RATS OF FOLLICLE-STIMULATING HORMONE DURING THE PERIOD OF OVULATION INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE

1979 ◽  
Vol 81 (1) ◽  
pp. 109-118 ◽  
Author(s):  
SHUJI SASAMOTO ◽  
SHIGEO HARADA ◽  
KAZUYOSHI TAYA
Keyword(s):  
Luteinizing Hormone ◽  
Plasma Concentrations ◽  
High Plasma ◽  
Oestrous Cycle ◽  
Prolonged Release ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Follicular Maturation ◽  
Lh Rh ◽  
Premature Ovulation

When 1·0 μg luteinizing hormone releasing hormone (LH-RH) was given i.v. three times at 1 h intervals from 17.00 to 19.00 h on the day of dioestrus (day 0) to regular 4 day cyclic rats, premature ovulation was induced the next morning (day 1) with the number of ova present comparable to normal spontaneous ovulation. The next spontaneous ovulation occurred on the morning of day 5, 4 days after premature ovulation induced by LH-RH. Plasma concentrations of FSH and LH showed transient rises and falls within 1 h of administration of LH-RH; concentrations of FSH in the plasma decreased from 20.00 h on day 0 but markedly increased again from 23.00 h on day 0 to 02.00 h on day 1 and these high levels persisted until 14.00 h on day 1, with only a small increase of plasma LH during this period. The duration of increased FSH release during premature ovulation induced by LH-RH treatment was 6 h longer than the FSH surge occurring after administration of HCG on day 0. Surges of gonadotrophin were absent on the afternoon of day 1 (the expected day of pro-oestrus) and the surges characteristic of pro-oestrus occurred on the afternoon of day 4 and ovulation followed the next morning. The pituitary content of FSH did not decrease despite persisting high plasma levels of FSH during premature ovulation induced by either LH-RH or HCG on day 0. The changes in uterine weight indicated that the pattern of oestrogen secretion from the day of premature ovulation induced by LH-RH to the day of the next spontaneous ovulation was similar to that of the normal 4 day oestrous cycle. When 10 i.u. HCG were given on day 0, an increase in oestrogen secretion occurred on day 2, 1 day earlier than in the group given LH-RH on day 0. This advancement of oestrogen secretion was assumed to be responsible for the gonadotrophin surges on day 3. Similar numbers of fully developed follicles were found by 17.00 h on day 2 after premature ovulation induced by either LH-RH or HCG, suggesting that the shorter surge of FSH during premature ovulation induced by HCG had no serious consequences on the initiation of follicular maturation for the succeeding oestrous cycle in these rats. Administration of LH-RH on day 0 had no direct effect on the FSH surge during premature ovulation. Secretory changes in the ovary during ovulation may be responsible for this prolonged selective release of FSH.

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