Non-pregnant Adult Rats Research Articles

Early Neurodevelopmental Anomalies in Young Rats from Adult female Treated with Valproic Acid

Background: the influence of VPA on murine fertility, and on offspring is well documented: VPA decreases the fertility rate (by 25%) and the number of fÅ“tus. Furthermore, VPA causes behavioral alterations in rodents similar to the symptoms observed in autism.Objective: in this study we investigated the effects of exposure of non-pregnant adult rats to VPA in the offspring of these animals.Material and methods: non-pregnant adult rats were divided into 3 groups; (1) distilled water group, (2) VPA 200 mg / kg group and (3) VPA 400 mg/kg group. The products were administered orally daily for 30 days. At the end of treatments, all rats were put into monogamous mating with breeding males. The zootechnical characteristics (gestation period, litter size, mortality rate) were then noted. The young rats were then subjected to a battery of behavioral tests (reversal and anti-gravity reflexes, cliff avoidance, suspension, motor coordination and eye opening), carried out at different stages of life to assess sensorimotor development. Morphological abnormalities were also sought, as well as the mortality rate on the 28th day of life.Results: An increase in the mortality rate and a decrease in the mean lifespan were found in female rats exposed to VPA. Young rats from female rats exposed to VPA showed decreased success rates and performance in behavioral testing. Morphodevelopmental abnormalities such as adictalia or stump necrosis were found in the VPA groups. The offspring mortality rate of female rats exposed to VPA 200 mg/kg was 100%.Conclusion: VPA administered to non-pregnant adult rats causes developmental abnormalities, decreased success rates for performance testing, deformities and increased mortality in young rats from the treated rats by VPA. Â

Afferent fibers involved in the bradykinin-induced cardiovascular reflexes from the ovary in rats.

Bleeding or rupture of the ovary often accompanies ovarian cysts and causes severe pain and autonomic responses such as hypotension. It would be expected that ovarian afferents contribute to cardiovascular responses induced by ovarian failure. The present study examined cardiovascular responses to noxious chemical stimulation of the ovary by bradykinin, an algesic substance released by tissue damage, and explored the role of ovarian afferents in the ovarian-cardiovascular responses in anesthetized rats. Non-pregnant adult rats were anesthetized with pentobarbital and artificially ventilated. The carotid artery was cannulated to monitor blood pressure and heart rate. Noxious chemical stimulation was achieved by applying a small piece of cotton soaked with bradykinin to the surface of the ovary for 30s. Application of bradykinin (10(-4) M) to the ovary decreased heart rate and blood pressure. These cardiovascular responses were not significantly influenced by severance of the vagal nerves or the superior ovarian nerve, but were abolished by severance of the ovarian nerve plexus (ONP). Application of bradykinin (10(-4) M) to the ovary evoked afferent activity of the ONP both in vivo and in vitro preparations. These results indicate that the decreases in heart rate and blood pressure following chemical noxious stimulation of the ovary with bradykinin are reflex responses, whose afferent nerve pathway is mainly through afferent fibers in the ONP.

Expression of sperm protein 22 (SP22) in the rat ovary during different reproductive states.

Sperm protein 22 (SP22) is correlated with fertility in rats. It has been identified in testis and implicated in sperm-egg interaction, protection against oxidative stress, and androgen receptor function. SP22 is widespread in rat and human tissues but has not yet been reported in the ovary. Using reverse transcription polymerase chain reaction, we identified the presence of SP22 transcripts in the rat ovary. We assessed the cellular distribution of the SP22 protein by collecting ovaries from rats in each of the following groups: 30, 60, and 90 days old; Days 9.5, 14.5, 16.5, 18.5, and 20.5 of pregnancy; and Days 1, 2, 8, and 19 of lactation. Tissue sections were stained immunohistochemically for SP22, and some serial sections were stained for relaxin or cytochrome P450 cholesterol side-chain cleavage enzyme (SCC). Weak staining for SP22 was evident in some corpora lutea (CL) and some interstitial gland cells in nonpregnant adult rats. At Day 9.5 of pregnancy, SP22 was detected in all CL, but staining intensity was weak. Staining intensity for SP22 in CL increased from Day 9.5 to 20.5 of pregnancy but was low on postpartum Day 1 and thereafter. A similar temporal pattern of staining intensity in CL was observed for relaxin. Strong immunoreactivity for SCC was present in the CL throughout pregnancy, and the spatial distribution of staining for SP22 in CL and in some areas of ovarian stroma was similar to that for SCC. There was weak staining of some theca cells in some antral follicles of pregnant and early postpartum rats when heat-induced antigen retrieval was used. There was inconsistent staining of oocytes for SP22, particularly in 30-day-old rats. In summary, the expression of SP22 was most prevalent in the CL and increased during pregnancy.

Progesterone increases Ca2+ currents in myometrial cells from immature and nonpregnant adult rats.

We examined the role of ovarian steroids in regulating Ca2+ channels in rat uterine smooth muscle. Ca2+ currents (ICa) in myometrial cells from nonpregnant adult rats and immature rats injected with either estrogen or progesterone or estrogen plus progesterone were measured with the whole cell patch-clamp method. ICa was more prominent in cells from diestrous rats than in cells from estrous rats. In cells from immature rats the ICa density was significantly greater in cells from progesterone-injected rats than in cells from estrogen-injected or noninjected rats. ICa in cells from rats injected simultaneously with progesterone and the progesterone antagonist RU-486 was not significantly greater than those from noninjected rats. These increases in ICa density are not the result of changes in ICa activation kinetics or voltage dependence, since both are unaffected by steroid injection. The kinetics and voltage dependence of the ICa current in cells from immature and nonpregnant adult rats are similar, suggesting that they represent a single population of Ca2+ channels.

Structure and function of phosphatidylglycerol-deficient lung surfactant.

The structure and properties of phosphatidylglycerol-deficient lung surfactant were examined using the myoinositol-treated rat as an experimental model. Hyperinositolemia was produced in pregnant rats (and their fetuses) by the administration of myoinositol throughout the final 5 days of gestation. Weight gain by pregnant rats during this period was reduced significantly as a result of myoinositol treatment. On day 21 of gestation, the number of type II cells in sections of lungs from fetuses of myoinositol-treated rats was not significantly different from that of fetuses of saline-treated rats. The profile area occupied by lamellar bodies, however, was significantly decreased in type II cells of fetuses from myoinositol-treated rats. There also was an apparent decrease in the size of lamellar bodies in the lungs of hyperinositolemic fetuses, but this was not accompanied by alterations in the structure of the tubular myelin form of surfactant present in fetal alveoli. Nonpregnant adult rats treated with myoinositol exhibited no gross respiratory impairment, and the recovery of total phospholipid in their alveolar lavage fluid was indistinguishable from that of saline-treated rats. In contrast, the phosphatidylglycerol content of the lavage fluid was decreased and the phosphatidylinositol content was increased as a result of myoinositol treatment. Furthermore, the molar ratio of palmitate to stearate esterified in phosphatidylglycerol was decreased (from 6.2 to 1.4) after myoinositol treatment. The palmitate/stearate ratio for phosphatidylinositol, however, tended to increase after myoinositol treatment. Pressure-volume relationships for freshly excised lungs of myoinositol-treated rats were not significantly different from those for lungs of saline-treated rats. Similarly, the surface-active properties of phosphatidylglycerol-deficient surfactant, measured in vitro by use of a surface balance, were not different from those of normal surfactant. These data indicate that phosphatidylglycerol-deficient surfactant has normal surface activity, and that the apparent requirement for phosphatidyglycerol for normal respiration in the neonate is likely not related directly to surface activity.

UDP-galactose:Glycoprotein galactosyltransferase activity in tissues of developing rat

UDP-galactose:glycoprotein galactosyltransferase activity has been measured in several tissues of the rat, ranging in age from 16 days embryo to 35 days postnatal. The enzyme activity was found to be high in fetal liver, lungs, and brain tissues but the concentration decreased with gestational age with no further changes after birth. The enzyme activity in the serum of newborns was higher than in pregnant and nonpregnant adult rats. There was no qualitative difference (optimum pH, cation requirements, affinity for the substrate UDP-galactose, or requirement for Triton X-100) between the enzyme from embryonic liver and that from adult rats. During the embryonic stage nearly half of the enzyme activity was localized in a plasma membrane-rich fraction and only a minor part in the microsomal fraction, while in the adult most of the activity was present in the microsomal fraction. Under certain conditions of assay the incorporation of galactose into glycoprotein in liver homogenates was greatly stimulated by CDP-choline or ATP. However, CDP-choline showed a considerably greater effect than ATP at 5 days after birth but this effect could be eliminated by solubilizing the homogenates in deoxycholate.