FESCUE INDUCED INHIBITION OF PROLACTIN SECRETION: DEVELOPMENT OF A RAT MODEL (RADIOIMMUNOASSAY, IMMUNOCYTOCHEMISTRY, ELECTRON MICROSCOPY)

Effects of Kentucky-31 endophyte-infected seed extract (KEISE) on serum and plasma prolactin (PRL), on hypophyseal concentrations of PRL and the ultrastructure of hypophyseal and mammary glands were investigated. Time-bred Sprague-Dawley rats received chronic levels of KEISE or PSS over a period of 10 d. The KEISE-treated dams did not produce a rise in serum PRL after whelping and were agalactic. Pups were either stillborn or small and weak and usually starved to death. PSS-treated dams produced normal elevations in serum PRL after whelping, supplying copious amounts of milk to large, healthy litters. Student's T test indicated no difference between control and treated rats on d 16 and 18 and differences on d 20, 22, 24, and 26. Dunnett's test indicated treatment means for control rats differed from control means all days except d 16. Treatment means for KEISE-treated rats did not differ from control mean.;Prolactin was immunocytochemically stained in hypophyseal tissue and evaluated with a microspectrophotometer. Absorbance in KEISE-treated animals was 22% while PSS-treated animals absorbed 37%, a substantial difference at the 95% confidence level.;Hypophyseal and mammary tissues from KEISE and PSS-treated synchronized-bred nursing rats were studied ultrastructurally. PRL-producing cells from KEISE-treated rats showed decreased rough endoplasmic reticulum (RER), Golgi apparatus (GA), ribosomes and immature and mature secretory granules compared to control cells. The mammary gland in KEISE-treated rats contained noticeable differences in RER and GA when compared to controls and secretory vesicles increased confirming a lack of secretion.;Non-pregnant rats with heterogeneous hypophyseal grafts (HAG) were used to produce artificially high levels of PRL to observe the effects of KEISE on plasma PRL. A single dose of 4.86 gram seed equivalents/milliliter (g sd eg/ml) of KEISE produced a decrease in PRL for 3 to 6 h, then rebounded to the original zero levels. Plasma PRL in PSS-treated rats remained constant throughout the experiment. The pattern across time differed significantly (P < .05). A dose response using PRL and KEISE was observed in the HAG rats. Plasma PRL levels decreased as a linear function of increasing KEISE dose levels (30 min: P < 0.03 and 60 min: P < 0.01).