The mammalian heart is known to undergo significant mechanical changes during fetal and neonatal development. The objective of this study was to define the ontogeny of the ryanodine receptor/$Ca^{2+}$ release channel and SERCA that play the major roles in excitation-contraction coupling. Whole ventricular homogenates of fetal (F) (19 and 22 days in gestation), postnatal (N) (1 and 7 days postnatal), and adult (A) (5 weeks postnatal) Sprague-Dawley rat hearts were used to study [$^3H$]ryanodine binding and oxalate-supported $^{45}Ca^{2+}$ uptake. For the ryanodine receptor, the major findings were: (1) The ryanodine receptor density, as determined by maximal [$^3H$]ryanodine binding ($B_{max}$), increased 3 fold between the F22 and A periods ($0.26{\pm}0.1$ vs. $0.73{\pm}0.07$ pmoles/mg protein, p<0.01), whereas there was no significant change during the F22 and N1 development phases ($0.26{\pm}0.1$ vs. $0.34{\pm}0.01$). (2) Affinity of the ryanodine receptor to ryanodine did not significantly change, as suggested by the lack of change in the $K_d$ during the development and maturation. For SERCA, changes started early with an increased rate of $Ca^{2+}$ uptake in the fetal periods (F19: $8.1{\pm}1.1$ vs. F22: $19.3{\pm}2.2$ nmoles/g protein/min; p<0.05) and peaked by 7 days (N7) of the postnatal age ($34.9{\pm}2.1$). Thus, we conclude that the quantitative changes occur in the ryanodine receptor during myocardial development. Also, the maturation of the $Ca^{2+}$ uptake appears to start earlier than that of the $Ca^{2+}$ release.
Purpose: This study aimed to investigate the relative weight gain at 2-week intervals up to 6 weeks after birth to predict retinopathy of prematurity (ROP) requiring treatment among very low birth weight infants. Methods: A total of 211 preterm infants with birth weights <1,500 g and gestational age <32 weeks were retrospectively reviewed. The main outcome was the development of ROP requiring treatment. Body weight measurements were recorded daily. Relative weight gains (g/kg/day) were calculated at the second, fourth, and sixth week after birth. Results: Of the 211 infants, 89 developed ROP, of which 41 spontaneously regressed and 48 with early treatment of ROP type I required laser treatment. The relative weight gain at 2, 4, and 6 weeks postnatal age was significantly lower in infants with ROP requiring treatment than in infants without ROP or those with spontaneous regression (P<0.001, P=0.005, and P=0.004, respectively). On logistic regression, poor relative weight gain in the first 2 weeks was found to be related to ROP requiring treatment (adjusted odds ratio, 0.809; 95% confidence interval, 0.695-0.941; P=0.006). Relative weight gain at 2 weeks postnatal age was significantly lower in infants with ROP requiring treatment compared to that in ROP requiring no treatment (P=0.012). Conclusion: Poor postnatal weight gain in the first 2 weeks of life is an important and independent risk factor for ROP requiring treatment. Postnatal weight gain can predict the development of severe ROP requiring treatment.
To learn the developmental changes in intrinsic electrophysiological properties of the second order taste neurons, whole cell recordings from the developing nucleus of the solitary tract neurons were done in brainstem slices of postnatal rats. Rats aged from postnatal 0 to 21 days (P0-P21) were used, being divided into 3 age groups: postnatal first week (P0-P7 days), second week (P8-P14 days), and third week (P15-P21 days). Slices containing gustatory NTS were cut horizontally in the thickness of $300\;{\mu}m.$ Whole cell recordings were obtained from neurons in response to a series of hyperpolarizing and depolarizing current pulses. The intrinsic electrophysiological properties of the rostral NTS (rNTS) neurons were compared among the age groups. Depolarizing current pulses evoked a train of action potentials in all neurons of all age groups. The resting membrane potential and input resistance of the neurons did not show any significant differences during the postnatal 3 weeks. The time constant, however, decreased during the development. Duration of action potential measured at half maximum amplitude was longer in younger age groups. Both the maximum rate of rise and the maximum rate of fall in the action potential increased during the first 3 weeks postnatal. Electrophysiologically more than half neurons were type III. In summary, it is suggested that developmental changes in electrophysiological properties in rNTS occur during the first three weeks in rats.
Seo, Hee-Jung;Lee, Seong-Kyu;Baik, Haing-Woon;Lee, Ki-Ho
Journal of Animal Science and Technology
/
v.54
no.3
/
pp.157-163
/
2012
The male reproduction is precisely controlled by a number of intrinsic and extrinsic factors. These factors usually involve in expressional regulation of various molecules influencing on sperm production in the testis. A number of ways are employed to control the transcription of specific genes, including epigenetic modifications of DNA and histone molecules. DNA methylation of CpG dinucleotides is a commonly used regulatory mechanism for testicular genes associated with the fertility. Previous studies have demonstrated the infertility induced by improper DNA methylation of these genes. In the present research, we attempted to determine transcriptional expression of some of these genes in the rat testis at different postnatal ages using real-time PCR analysis. These genes include neurotrophin 3 (Ntf3), insulin-like growth factor II (Igf2), JmjC-domain-containing histone demethylase 2A 1 (Jhm2da), paired box 8 transcription factor (Pax8), small nuclear ribonucleoprotein polypeptide N (Snrpn), and 5,10-methylenetetrahydrofolate reductase (Mthfr). The expression levels of Ntf3, Igf2, and Snrpn genes were the highest at the neonatal age, followed by transient decreases at the prepubertal age. Expression of Jhm2da and Mthfr genes were continuously increased from the neonate to 1 year of age. The levels of Pax8 mRNA at the early ages were higher than those at the later ages of postnatal development. These findings suggest that expression of some fertility-associated testicular genes in the rat during postnatal period could be differentially regulated by the control of the degree of DNA methylation.
A cell frequently utilizes glucose as a fuel of energy and a major substrate of lipid and protein syntheses. A regulation of glucose movement into and out of the cells is precisely controlled by cooperative works of passive and sodium-dependent active processes. At least 13 glucose cotransporter (Slc2a, GLUT) isoforms involve in passive movement of glucose in cells. The efferent ductules (EDs) play in a number of important functions for maintenance of male fertility. In the present study, using real-time PCR analysis, we determined gene expression of five Slc2a isoforms in the EDs. In addition, we compared expression levels of these Slc2a isoforms according to postnatal development ages, 1 week, 2 weeks, 1 month, and 3 months. Results from the current study showed that expression of Slc2a1, Slc2a3, and Slc2a5 mRNAs reached the highest levels at 1 month of age, followed by a transient decrease at 3 months of age. In addition, the level of Slc2a4 mRNA reminded at steady until 1 month of age and was significantly reduced at 3 months of age, whereas the highest level of Slc2a 8 mRNA was detected at 2 weeks of age. Data from the present study indicate a differential expression of various Slc2a isoforms in the ED according to postnatal ages. Thus, it is believed that glucose movement through the epithelial cells in the ED would be regulated by the coordinated manner among Slc2a isoforms expressed at a given age.
Glucose is a major source of metabolic fuel and lipid and protein syntheses. Transport of glucose into the cell is regulated by an action of glucose transport.associated transporters, especially solute carriers 2A (Slc2a, protein symbol GLUT). The present study was focused on examination of mRNA expression of various Slc2a isoforms in the epididymis during postnatal development. Total RNAs isolated from different epididymal segments (caput, corpus, and caudal epididymis) were utilized for real-time polymerase chain reaction analyses. Results showed that Slc2a 1, 3, 4, 5, and 8 were expressed in the entire epididymal regions. In addition, the abundance of these Slc2a isoforms' transcripts was different within each epididymal regions. Moreover, the present study showed differential expression of these Slc2a isoforms among different epididymal segments according to postnatal ages. The current study suggests that glucose transport in the epididymis via various Slc2a isoforms would be necessary for maintenance of the epididymal functions.
The purpose of this study was to test that motor skill training enhance motor function and cerebellar development. Using an animal model of fetal alcohol syndrome-which equates peak blood alcohol concentrations across developmental period-critifical periods for the effect of alcohol on body and cerebellar weigh was examined. The effect of motor skill training on motor function and cerebellar development of rat exposed alcohol on postnatal days 4 through 10 were studied. Newborn rats were assigned to one of two groups: (1) Control group (CG), via artificial rearing to milk formula and (2) experimental groups (EG), via 4.5g/kg/day of ethanol in a milk solution. After completion of the treatments, the pups were fostered back to lactating dams, and wearing they were raised in standard caged until they were postnatal 48 days. Rats from experimental group of postnatal treatment then spent 10 days in one of two groups: Experimental group II (EGII) was had got motor skill training (training traverse a set of 6 elevated obstacles) for 4 weeks. Experimental group I (EGI) was not trained. Before sacrificing, the rat got examined two behavioral test, body weigh and cerebellar weigh, then coronal sections were processed. The section was investigated the Purkije cell in the cerebellum using light microscope. The results of this study were as follows. 1. In body weight test, the outcome of alcohol groups were significantly lower than the normal group. 2. In cerebellar weight test, the outcome of EGI were significantly lower than CG and EGII. 3. In motor behavioral test, the outcome of EGI was significantly lower than NG and EGII. 4. In Purkinje cells counting test, the outcome of EGI was significantly lower than the NG and EGII. These result suggest that improved motor function induced by motor skill training after postnatal exposure is associated with dynamically altered expression of Purkinje cells and that is related with cerebellar function. Also, these data can potentially serve as a model for therapeutic intervention.
Background: Animal studies have shown that a leukocyte influx precedes the development of bronchopulmonary dysplasia (BPD) in premature sheep. The CXC chemokine receptor 2 (CXCR2) pathway has been implicated in the pathogenesis of BPD because of the predominance of CXCR2 ligands in tracheal aspirates of preterm infants who later developed BPD. Purpose: To test the effect of CXCR2 antagonist on postnatal systemic and pulmonary inflammation and alveolarization in a newborn Sprague-Dawley rat model of BPD. Methods: Lipopolysaccharide (LPS) was injected intraperitoneally (i.p.) into the newborn rats on postnatal day 1 (P1), P3, and P5 to induce systemic inflammation and inhibit alveolarization. In the same time with LPS administration, CXCR2 antagonist (SB-265610) or vehicle was injected i.p. to investigate whether CXCR2 antagonist can alleviate the detrimental effect of LPS on alveolarization by attenuating inflammation. On P7 and P14, bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) were collected from the pups. To assess alveolarization, mean cord length and alveolar surface area were measured on 4 random nonoverlapping fields per animal in 2 distal lung sections at ×100 magnification. Results: Early postnatal LPS administration significantly increased neutrophil counts in BALF and PB and inhibited alveolarization, which was indicated by a greater mean cord length and lesser alveolar surface area. CXCR2 antagonist significantly attenuated the increase of neutrophil counts in BALF and PB and restored alveolarization as indicated by a decreased mean cord length and increased alveolar surface area in rat pups exposed to early postnatal systemic LPS. Conclusion: CXCR2 antagonist preserved alveolarization by alleviating pulmonary and systemic inflammation induced by early postnatal systemic LPS administration. These results suggest that CXCR2 antagonist can be considered a potential therapeutic agent for BPD that results from disrupted alveolarization induced by inflammation.
A perinatal and postnatal study of KTC-1, a new semisyntheitic rifamycin antituberculous drug, was conducted in Sprague-Dawley rats. Dosages of KTC-1 0, 12, 27.6, and 63.5 mg/kg/day were administered to dams orally by gavage from day 17 of gestation to day 21 of lactation. All pregnant rats were allowed to deliver naturally for postnatal examination of their offspring. At 63.5 mg/kg/day, weakness, dark-red discharge around eyes, a loss in body weight, and a decrease in food and water consumption were observed in dams. An increase in the weight of adrenal gland and spleen, and a decrease in the weight of kidney and heart were also found. An increase in neonatal deaths during the lactation period, a loss in body weight, a delay in physical development, a decrease in traction ability, an increase in the number of errors and the time required for the multiple T-maze trial were found in F1 offspring. In addition, an increase in the incidence of visceral variations and retarded ossification were observed in F1 4 day old rats. An increase in the incience of skeletal anomalies was seen in F2 fetuses. There were no sings of maternal toxicity or embryotoxicity at 12 and 27.6 mg/kg/day. From the results mentioned above, it can be concluded that the no-effect dose levels(NOELs)for dams, F1 offspring, and F2 fetuses are 27.6 mg/kg/day.
The coordinated action of the detrusor muscle cells in the urinary bladder is governed by cell-cell communication through gap junction, consisted of connexin (Cx) molecules. Even though a number of researches have been mostly focused on expressional changes of a few Cx isoforms in clinically dysfunctional condition of the bladder, less attention has been paid for investigation of Cx isoforms present in the bladder. Using real-time PCR analysis, the present study examined Cx isoforms expressing in the male rat bladder during postnatal period. Also, expressional patterns of Cx isoforms were evaluated in the bladder at different postnatal ages. Of a total of 13 Cx isoforms tested in the present study, we were able to detect mRNAs of 6 Cx isoforms in the rat urinary bladder, including Cxs 31, 31.1, 32, 37, 40, and 45. The transcript levels of Cxs 31, 31.1, 37, 40, and 45 were gradually increased from 1 week of age until 25 days of age, followed by transient decreases at 45 days of age. However, abundance of Cx32 transcript was drastically increased at 15 days of age, followed by a sharp drop at 45 days of age. These results indicate that differential expression of Cx isoforms in the bladder during postnatal development would be necessary for maintaining proper function of the bladder. A question remains to be answered if significant decreases of transcript levels of some Cx isoforms at the elderly are associated with age-dependent dysfunction of the bladder.
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