TY - JOUR
T1 - Neuroendocrine control of gonadotropin secretion
AU - Porter, J. C.
AU - Nansel, D. D.
AU - Gudelsky, G. A.
AU - Foreman, M. M.
AU - Pilotte, N. S.
AU - Parker, C. R.
AU - Burrows, G. H.
AU - Bates, G. W.
AU - Madden, J. D.
PY - 1980
Y1 - 1980
N2 - Luteinizing hormone releasing hormone (LHRH), a hypothalamic peptide that is concentrated in granules of neurons, has the capacity to release gonadotropins (Luteinizing hormone (LH) and follicle stimulating hormone) from the pituitary gland. LHRH has been found in hypophysial portal blood of rats, monkeys, and rabbits. Antibodies to LHRH depress plasma LH concentrations in castrated animals and evoke testicular atrophy, but passive immunization against LHRH does not block the LH surge induced by estrogen in monkeys. Estrogens, progestin, prolactin, and dopamine have marked effects on LH secretion, yet an association between these effects and altered hypophysial portal blood concentrations of LHRH is not established. In view of the paucity of evidence demonstrating such a cause and effect relationship, two alternative proposals have become tenable. One, hormones and neurotransmitters may not alter the levels of portal blood LHRH, but rather alter the frequency of pulsatile LHRH secretion. Two, hormones, such as estrogens, progesterone, and prolactin, may alter the responsiveness of the gonadotropin-secreting cells to LHRH by affecting the secretion of dopamine.
AB - Luteinizing hormone releasing hormone (LHRH), a hypothalamic peptide that is concentrated in granules of neurons, has the capacity to release gonadotropins (Luteinizing hormone (LH) and follicle stimulating hormone) from the pituitary gland. LHRH has been found in hypophysial portal blood of rats, monkeys, and rabbits. Antibodies to LHRH depress plasma LH concentrations in castrated animals and evoke testicular atrophy, but passive immunization against LHRH does not block the LH surge induced by estrogen in monkeys. Estrogens, progestin, prolactin, and dopamine have marked effects on LH secretion, yet an association between these effects and altered hypophysial portal blood concentrations of LHRH is not established. In view of the paucity of evidence demonstrating such a cause and effect relationship, two alternative proposals have become tenable. One, hormones and neurotransmitters may not alter the levels of portal blood LHRH, but rather alter the frequency of pulsatile LHRH secretion. Two, hormones, such as estrogens, progesterone, and prolactin, may alter the responsiveness of the gonadotropin-secreting cells to LHRH by affecting the secretion of dopamine.
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M3 - Article
C2 - 6773815
AN - SCOPUS:0019184294
SN - 0014-9446
VL - 39
SP - 2896
EP - 2901
JO - Federation Proceedings
JF - Federation Proceedings
IS - 11
ER -