Attenuation of endogenous opioid peptide inhibition of [Gln8]luteinizing hormone-releasing hormone secretion during sexual maturation in the cockerel.
Opiatergic inhibition of [Gln8]LHRH secretion from the mediobasal hypothalamus of the cockerel (Gallus domesticus) was studied during sexual maturation in a hypothalamic superfusion system. The basal and depolarization-induced release of [Gln8]LHRH in the presence and absence of the opiate agonists [D-Ala2,N-Phe4-Gly-ol5]enkephalin (DAGO), which binds selectively to the mu-receptor subtype, and [D-Thr2,L-Leu5] enkephalyl-Thr (DTLET), which binds selectively to the delta-receptor subtype, and of the opiate antagonist naloxone was assessed in tissue obtained from birds at 4, 8, 12, 16, 20, and 24 weeks of age. Concentrations of LH and testosterone in plasma obtained from cockerels at the same ages rose progressively from 8-16 weeks of age. Between 16 and 20 weeks of age testosterone increased about 3-fold, whereas LH decreased significantly. Thereafter, LH rose in the face of sustained plasma testosterone concentrations. The initial rise in plasma LH concentrations was associated with a rise in the basal release of [Gln8]LHRH and a decrease in the ability of DAGO to inhibit and of naloxone to stimulate [Gln8]LHRH release. The delta-agonist DTLET did not affect secretion at any time. The fall in plasma LH at 20 weeks occurred despite an increased release of [Gln8]LHRH, whereas the subsequent rise in LH release occurred at a time when the pattern of [Gln8]LHRH release remained unchanged. These observations support the proposition that a decrease in tonic opioid inhibition of [Gln8]LHRH secretion during sexual maturation may explain why plasma LH concentrations rise in the face of sustained plasma testosterone concentrations. The changes in plasma LH concentrations that occur in the immediate pubertal period may be due, however, to a direct action of testosterone on the anterior pituitary lobe.
Stansfield
S C
SC
Department of Physiology and Biochemistry, University of Reading, Whiteknights, United Kingdom.
Cunningham
F J
FJ
D000818:Animals; D002645:Chickens / Q000502:physiology*; D004723:Endorphins / Q000502:physiology*; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D004745:Enkephalins / Q000494:pharmacology; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives* / Q000378:metabolism; D007033:Hypothalamus, Middle / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D009842:Oligopeptides / Q000494:pharmacology; D011761:Pyrrolidonecarboxylic Acid / Q000031:analogs & derivatives; D012741:Sexual Maturation; D013739:Testosterone / Q000097:blood
D004723:Endorphins; D004745:Enkephalins; D009842:Oligopeptides; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D007987:Gonadotropin-Releasing Hormone; D009270:Naloxone; D013739:Testosterone; C037700:LHRH, Gln(8)-; C037653:deltakephalin; D011761:Pyrrolidonecarboxylic Acid