The proestrous prolactin surge is not the sole initiator of regressive changes in corpora lutea of normally cycling rats.
During the estrous cycle, secretion of prolactin is largely restricted to a surge on proestrus. We investigated whether this proestrous prolactin surge initiates regression of the corpora lutea of the preceding cycle. Adult rats were killed prior to the prolactin surge (Proestrus group), following the prolactin surge (Estrus group), after chemical blockade of the prolactin surge with bromocryptine (Estrus+BRC group), and after blockade of the prolactin surge and administration of prolactin (Estrus+BRC+PRL group). Corpora lutea of the current (proestrus) or preceding (estrus) cycle were dissected out, weighed, and sectioned for immunohistochemistry or cultured for examination of in vitro progestin production. Numbers of luteal monocytes/macrophages, differentiated macrophages, and apoptotic nuclei per high-power field were greater for Estrus and Estrus+BRC+PRL than for Estrus+BRC, which in turn had greater numbers than Proestrus (P< 0.05). In contrast, BRC completely reversed the decline in luteal weight observed between Proestrus and Estrus (P<0.05). Number of major histocompatibility complex II-positive cells was not different between groups (P>0.05). Finally, progestin production by corpora lutea in vitro was lower for Proestrus than for the other groups (P<0.05). The results indicate that the prolactin surge alone is not responsible for initiation of apoptosis or immune cell infiltration in regressing corpora lutea of the estrous cycle, although prolactin increases these markers of regression. Prolactin does cause a decline in luteal weight; however, the corpora lutea retain the capacity for steroidogenesis. We conclude that although prolactin has a role in luteal regression, it is not solely responsible for the initiation of this process.
Bowen
J M
JM
Department of Physiology and Reproductive Sciences Program, University of Michigan, Ann Arbor, Michigan 48109, USA. bowenjm@umich.edu
Keyes
P L
PL
D004092:20-alpha-Dihydroprogesterone / Q000096:biosynthesis; D000818:Animals; D000911:Antibodies, Monoclonal; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D001971:Bromocriptine / Q000494:pharmacology; D002467:Cell Nucleus / Q000187:drug effects / Q000648:ultrastructure; D004971:Estrus / Q000502:physiology*; D005260:Female; D005802:Genes, MHC Class II / Q000276:immunology; D006727:Hormone Antagonists / Q000494:pharmacology; D007150:Immunohistochemistry; D003341:Luteolysis / Q000502:physiology*; D008264:Macrophages / Q000187:drug effects / Q000648:ultrastructure; D011359:Proestrus / Q000097:blood / Q000502:physiology*; D011374:Progesterone / Q000096:biosynthesis; D011388:Prolactin / Q000037:antagonists & inhibitors / Q000494:pharmacology / Q000502:physiology*; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley
D000911:Antibodies, Monoclonal; D006727:Hormone Antagonists; D004092:20-alpha-Dihydroprogesterone; D001971:Bromocriptine; D011374:Progesterone; D011388:Prolactin