An analysis of physiological mechanisms underlying the antigonadotropic action of intracranial prolactin in ring doves.
Intracerebroventricular (ICV) injections of prolactin (PRL) exert potent antigonadal and antigonadotropic effects in ring doves (Streptopelia risoria) at doses that are insufficient to stimulate prolactin-dependent crop growth. To explore the physiological basis of these effects, we tested the ability of ICV-injected PRL to influence pituitary responsiveness to chicken gonadotropin-releasing hormone-I (cGnRH-I) and to alter GnRH content and concentration in the preoptic area (POA) and median eminence (ME). cGnRH-I-induced changes in plasma LH were monitored by radioimmunoassay (RIA) in photostimulated male doves after they received five daily ICV injections of ovine PRL (1 microg/2 microl) or saline vehicle. Although PRL treatment reduced basal plasma LH levels and testes weight, it did not reduce the amount or alter the pattern of LH released in response to a bolus injection of cGnRH-I. This suggests that ICV PRL does not suppress LH by reducing pituitary responsiveness to GnRH. In two subsequent studies, GnRH content (ng/region) and concentration (pg/microg protein) in the POA and ME were measured in male doves by RIA and by competitive enzyme immunoassay after 5 days of ICV PRL or vehicle treatment. Although ICV PRL reduced plasma LH levels in both studies, no significant PRL-induced alterations in GnRH content or concentration were apparent. In a final study, PRL-treated female doves had lower plasma LH levels than vehicle-treated control females at 12 and 24 h after a single ICV injection. GnRH content of the POA was also lower in PRL-treated females than in controls at 24 h. However, the two treatment groups did not differ in POA or ME GnRH content at earlier postinjection sampling intervals. Analysis of GnRH concentration data revealed no treatment group differences in either region at any sampling interval (1, 6, 12, or 24 h post-PRL injection). Collectively, these results are consistent with the idea that ICV-injected PRL acts at the level of the CNS to inhibit the reproductive system. However, the nature of the alterations involved remains to be clarified. Plausible hypotheses are (1) that ICV PRL suppresses the gonadal axis by influencing the activity of GnRH neurons at brain sites other than the POA or ME or (2) that PRL alters the synthesis, storage, degradation, and/or release of GnRH in the POA or ME, but the dynamic changes involved are not reflected in integrated, steady-state measures such as peptide content or concentration in tissue.
Buntin
J D
JD
Department of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53201, USA.
Advis
J P
JP
Ottinger
M A
MA
Lea
R W
RW
Sharp
P J
PJ
D000818:Animals; D010856:Columbidae / Q000502:physiology*; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000097:blood; D007276:Injections, Intraventricular; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008473:Median Eminence / Q000187:drug effects / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism; D011301:Preoptic Area / Q000187:drug effects / Q000378:metabolism; D011388:Prolactin / Q000008:administration & dosage* / Q000494:pharmacology*; D013737:Testis / Q000187:drug effects
D007987:Gonadotropin-Releasing Hormone; D011388:Prolactin; D007986:Luteinizing Hormone