Apoptosis, therefore, may occur first in response to a prolactin signal and then be perpetuated in the regressing tissue by the actions of macrophages that are also recruited in response to the prolactin signal. Evidence for continued tissue deletion after repeated exposures to prolactin is provided by the whole ovarian sections (experiment 1), in which corpora lutea of several different ages and regressive states were present. In these sections, despite this heterogeneity, a significant increase in apoptotic nuclei per high-power field was seen on the morning of estrus as compared to proestrus, and this increase was remarkably similar to that seen in corpora lutea first entering regression on estrus (experiment 2). This suggests that each prolactin surge might initiate a new round of apoptosis in all regressing corpora lutea. antibiotic levaquin
If this is so, then administration of prolactin every 12 h, as carried out in previous experiments with hypophysectomized rats, may lead to a maximal rate of tissue deletion. While the non-ED2-positive macrophages recruited in response to prolactin are associated with rapid regression of the corpus luteum, when prolactin is delivered every 12 h, it is altogether possible that increased differentiation and activation of macrophages are required for similarly paced regression following one, solitary prolactin signal, as occurs on proestrus during the es-trous cycle.