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JM Bowen1 *, PL Keyes1 *
Dept of Physiology, University of Michigan, Ann Arbor, MI 1
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 corpora lutea (CL). Adult rats were killed prior to the prolactin surge (Proestrus), following the prolactin surge (Estrus), after chemical blockade of the prolactin surge with bromocryptine (Estrus+BRC), and after blockade of the prolactin surge and administration of prolactin (Estrus+BRC+PRL). CL of the current (Proestrus) or immediately preceding (Estrus) cycle were dissected out, weighed, and sectioned for immunohistochemistry, or incubated for measurement 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). Finally, progestin production by CL 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 CL of the estrous cycle, although prolactin increases these markers of regression. Prolactin does cause a decline in luteal weight, however the CL 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. [NIH HD33478].
This abstract is being presented on Tuesday, August 3 at 5:15 PM at Todd 216.