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BackgroundDegenerative effects of critical regulators of reproduction, the kisspeptin peptides, on cellular aspects of sexually immature male gonads are known but similar information on accessory sex glands remain elusive.MethodsPrepubertal laboratory rats were injected kisspeptin-10 at three different dosage concentrations (10 pg, 1 ng and 1 microgram) for a period of continuous 12 days at the rate of two doses per day. Control rats were maintained in parallel. The day following the end of the experimental period, seminal vesicles were removed and processed for light and electron microscopic examination using the standard methods. DNA damage was estimated by DNA ladder assay and DNA fragmentation assay.ResultsThe results demonstrated cellular degeneration. Epithelial cell height of seminal vesicles decreased significantly at all doses (P < 0.05). Marked decrease in epithelial folds was readily noticeable, while the lumen was dilated. Ultrastructural changes were characterized by dilatation of endoplasmic reticulum and Golgi complex, heterochromatization of nuclei, invagination of nuclear membranes and a decreased number of secretory granules. Percent DNA damage to the seminal vesicle was 19.54 +/- 1.98, 38.06 +/- 2.09 and 58.18 +/- 2.59 at 10 pg, 1 ng and 1 microgram doses respectively.ConclusionThe study reveals that continuous administration of kisspeptin does not lead to an early maturation but instead severe degeneration of sexually immature seminal vesicles.

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The effect of prenatal protein deprivation on the timing of neurogenesis and on the number of neurons generated in the locus coeruleus of the rat was studied. These neurons are of interest as their axon projections are involved in the earliest stages of cerebral cortical development. Dams were maintained on a 25% casein diet or a 6% casein diet five weeks prior to mating and the diets continued throughout the pregnancy. At birth, all pups were cross-fostered to dams on a 25% casein diet. BrDU, a thymidine analog that is incorporated into the nuclear DNA during the synthetic phase of the cell cycle, was used as a marker of the generation period. It was administered intraperitoneally (25 mg/kg body weight) on embryonic day 10, 11, 12, 13, or 14. On postnatal day 30, the brain stems were processed with BrDU immunocytochemistry to determine the relative number of neurons generated on each day, and with Nissl stain to determine the total number of neurons generated in the two groups. There were no significant differences between the two diet groups in the timing of their generation or in the total number of neurons generated, indicating a preservation of neurogenesis of these early generated neurons in these malnourished rats.

The effect of prenatal protein deprivation on timing of neurogenesis and on number of neurons generated in the serotonergic dorsal (DR) and median raphe (MR) nuclei of the rat was studied. These neurons are of interest because their neurogenesis occurs during the period of malnutrition and their axonal projections participate in the earliest stages of brain development. In this study, dams were maintained on a 25% casein diet or a 6% casein diet 5 weeks prior to mating and throughout pregnancy. At birth, all pups were cross-fostered to dams on a 25% casein diet. Bromodeoxyuridine, a thymidine analog that is incorporated into nuclear deoxyribonucleic acid during the cell cycle synthetic phase, was used as a marker of neurogenesis. Bromodeoxyuridine was administered on either embryonic day 11, 12, 13 or 14. On postnatal day 30, serial sections of raphe nuclei were processed with bromodeoxyuridine immunocytochemistry to determine the number of raphe cells generated on each day and with Nissl stain to determine the total number of cells generated. There were no significant differences between the two diet groups in timing of generation or in total number of cells generated, indicating that neurogenesis of these early generated neurons appears unaffected by concomitant protein deprivation.