In this study we examined the effects of dopamine (DA) and its withdrawal on in vitro prolactin (PRL) release from subpopulations of lactotrophs from two regions of the anterior pituitary obtained from untreated ovariectomized (OVX) rats or OVX rats treated with estrogen, progesterone or a combination of the two. Anterior pituitaries were cut horizontally into an inner (dorsal) zone and an outer (ventral) zone. Each of these regions was enzymatically dispersed and the resulting cells were otherwise untreated (unseparated) or centrifuged through a discontinuous Percoll gradient to separate the cells into two subpopulations (light and heavy cells). Each of these types of cells was perifused for 1 h with culture medium containing 1 microM DA followed by medium devoid of DA for 1 h. Prolactin released into the perifusion medium, collected as 5-min fractions, was measured by radioimmunoassay and normalized to the number of lactotrophs in the cellular pools as determined by immunocytochemistry. In the presence of DA, PRL release from unseparated cells of the outer zone was significantly increased by estradiol treatment compared with the release from similar cells from OVX rats. (Differences were considered significant where P < 0.05.) However, no effect of estradiol treatment was observed with unseparated cells of the inner zone or light or heavy cells from either zone. Progesterone had no effect on any cell type when administered alone. However, when progesterone was given following estradiol, PRL release from unseparated cells of the inner zone was increased significantly compared with similar cells from the other steroid-treated groups. Similar significant increases were observed with light and heavy cells of the outer zone, but there was no effect of the combined steroid treatment on light or heavy cells from the inner zone. When DA was withdrawn, prolactin release was significantly increased from all cells except unseparated cells of the outer zone of OVX rat pituitaries. However, when the cells of the outer zone from OVX rats were separated into light and heavy cells, they responded to the withdrawal of DA with significant and equivalent increases in prolactin release. Light cells of the inner zone of pituitaries from OVX rats were more responsive to DA withdrawal than were heavy cells. Estradiol increased the response to the withdrawal of DA by light and heavy cells of the outer zone and heavy cells of the inner zone. Progesterone significantly reversed these effects of estradiol on separated cells. These results suggest that lactotrophs in two regions of rat pituitaries respond differently to dopamine and to its withdrawal, that subpopulations of lactotrophs within these regions also respond differently and that steroids modulate these responses.
This study was conducted to determine the plasma levels of prolactin in prepubertal and young, postpubertal, proestrus rats of mammary tumor-susceptible (Sprague-Dawley) and tumor-resistant (Long-Evans) strains using a sensitive bioassay-Nb2 lymphoma cell replication. Prepubertal Long-Evans rats had significantly higher levels of prolactin than did Holtzman Sprague-Dawley rats of the same age. Likewise, Long-Evans rats secreted significantly more prolactin into the blood on the afternoon and evening of proestrus than did Holtzman rats. Finally, ovariectomized Long-Evans rats released more prolactin into the blood at 1 day, but not at 8 or 15 days, of treatment with diethylstilbestrol. Prolactin levels determined by conventional radioimmunoassay and by bioassay were similar except on the afternoon of proestrus, when, in both strains of rats, the bioassay to radioimmunoassay ratio increased significantly above 1.0 during the late evening. In addition, the ratio was significantly less than 1.0 in the early and late afternoon in the Holtzman rats, but not Long-Evans rats. These data indicate that a strain of rats that is resistant to experimentally induced mammary cancer has higher prolactin levels in the blood than does a strain that is susceptible to mammary cancer at a time when mammary gland growth is rapid. Furthermore, there are times during the proestrus prolactin surge when the bioassay yielded higher and lower values of prolactin than radioimmunoassay of the same samples, suggesting functional heterogeneity of prolactin that may impact on mammary gland or other target tissue function.
The effect of thyroglobulin (Tg)iodination on the proliferation and suppression of thyroid-specific lymphocytes was examined in vivo in the obese strain (OS) and Cornell strain chicken models of autoimmune thyroiditis. Spleen cells from OS chickens were able to transfer disease to Cornell strain recipients. The ability to transfer disease was markedly reduced if the donors were raised on an iodine-depleting regimen. This deficiency was corrected by immunization of donor chickens with iodinated Tg. Immunization with low iodine Tg was ineffective. Neonatal tolerance induction with either iodinated or low iodine Tg reduced thyroiditis in 2-week-old OS chickens. Spleen cells from these tolerized chickens transferred to 4-day-old OS chickens were less thyroiditogenic. These results indicate that thyroid autoreactive cells are responsive to iodinated Tg, but not to low iodine Tg. Both of the Tg preparations, however, can induce tolerance to the disease. We conclude that distinct regions of the Tg molecule regulate the proliferation and suppression of thyroid-reactive lymphocytes, respectively. Only the former is dependent on the iodination of Tg. These results emphasize the importance of Tg as a self-antigen and provide one mechanism by which iodine may induce autoimmune thyroiditis.
The objective of this study was to determine the effects of thyrotropin-releasing hormone (TRH) and bromocriptine on plasma levels of biologically active prolactin in ovariectomized, diethylstilbestrol (DES)-treated rats. Female Long-Evans and Holtzman rats were ovariectomized and each was given a subcutaneous implant of diethylstilbestrol (DES). One week later, groups of DES-treated rats were fitted with indwelling intra-atrial catheters, and 2 days later blood samples were withdrawn before and at 1, 2, 5, 10, and 20 min after intravenous administration of TRH (250, 500, or 1000 ng/rat). Blood samples were obtained from other groups at 4 weeks of DES treatment by orbital sinus puncture under ether anesthesia before and at 30, 60, and 120 min after bromocriptine administration (2.5 mg/rat sc). Plasma was assayed for prolactin by conventional radioimmunoassay (RIA) and by Nb2 lymphoma bioassay (BA). Holtzman rats released significantly more prolactin following TRH than did Long-Evans rats when the RIA was used to measure prolactin. However, when the BA was used to assay prolactin in the same samples, the Long-Evans rats released more prolactin than did the Holtzman rats. In addition, the ratio of the BA to RIA values was significantly increased in both strains following TRH, but the greatest increase was observed in the Long-Evans rats, in which the ratio was 4.5 at the peak of the TRH-induced rise in plasma prolactin. Gel filtration chromatography of plasma obtained at 5 min after TRH treatment in Long-Evans rats revealed large molecular forms of prolactin with BA to RIA ratios of 4-5. In addition, monomeric prolactin had a BA to RIA ratio of 2. Bromocriptine treatment reduced prolactin levels in both strains, but the effect was more rapid in Holtzman than in Long-Evans rats. In addition, bromocriptine treatment of Holtzman, but not Long-Evans, rats significantly reduced the BA to RIA ratio of plasma prolactin. The results indicate that TRH and bromocriptine affect the release of biologically active prolactin to a greater extent than prolactin detected by antibody in the RIA, and that Long-Evans and Holtzman rats respond to these secretagogues differently with regard to BA to RIA comparisons.
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