Effects of maternal oral morphine consumption on neural tube development in Wistar rats

2005 ◽  
Vol 159 (1) ◽  
pp. 12-17 ◽  
Author(s):  
Shiva Nasiraei-Moghadam ◽  
Hedayat Sahraei ◽  
Hossein Bahadoran ◽  
Mehrangiz Sadooghi ◽  
Seyed Hossein Salimi ◽  
...  
1996 ◽  
Vol 78 (2) ◽  
pp. 391-400 ◽  
Author(s):  
B. F. Petrie

The role of differential housing on sucrose-morphine consumption in outbred Wistar rats was investigated in two studies. The results of earlier research, indicating rats housed in a quasinatural colony drank significantly less sucrose-morphine than rats isolated in standard laboratory cages, could not be replicated, as the consumption of sucrose-morphine by the isolated animals in the present two studies was reduced. It is possible that during a colony conversion the supplier inadvertently introduced strain differences making the present rats more resistant to xenobiotic consumption. Discussion documents the role of genetics in morphine consumption.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Leila Dehghani ◽  
Hedayat Sahraei ◽  
Rokhsareh Meamar ◽  
Masoomeh Kazemi

Previous studies have shown that morphine abuse during pregnancy cancause a delay in the development of the placenta and embryo and also bring about birth defects. The present study investigates the effect of the duration of maternal morphine consumption during pregnancy, as well as the impacts of morphine abuse on the development of placental layers during the three different periods of pregnancy in Wistar rats.Materials and Methodology. Female Wistar rats have been used in the present study. Experimental groups received morphine (0.05 mg/mL of drinking water) after one night of coupling with male rats for mating. On 9th, 10th, and 14th days of pregnancy, pregnant animals were killed, and placentas were removed and fixed. The cells of the placentas layers were calculated by light microscope and MOTIC and SPSS software.Results. The maternal surface thickness of the placenta was significantly increased, whereasthe fetal surface thickness of placenta was significantly decreased with morphine consumption with a time-dependent manner in experimental groups, compared to control groups. Moreover, the number of trophoblast cells increased in both maternal and fetal surfaces of placenta with respect to the duration of morphine consumption which was overt in the experimental groups compared to the control groups.Conclusion. In general, the time-dependent effects of oral morphine consumption can inhibit the development and natural functioning of cytotrophoblast and syncytiotrophoblast cells of the placental layers.


2021 ◽  
Author(s):  
Ting Li ◽  
Quan Huo ◽  
Zhi Guo Lu ◽  
Xin Ran Xing ◽  
Lu Ding ◽  
...  

Abstract Background The occurrence of neural tube defects is a complex process in which genes, internal and external environment and other factors jointly influence and occur interactively. In this experiment, animal models of different energy balance states are constructed. To explore the mechanism of fos and leptin-leptin receptor during neural tube development of offspring under different energy states and its effect on neural tube development of offspringMethods Using gene identification technology to obtain Mex3c+/- negative energy balance mice and high-fat diet to obtain positive energy balance mice, and obtain E10.5d, E12.5d, E14.5d embryos. We will verify the expression of fos, leptin, LEPR, nestin, PAX3, and H3K27me3 proteins in the neural tube of the offspring through relevant experimental methods.Results We have successfully constructed animal models, Control group (18.82g±1.54g), Mex3c group (18.84g±1.08g), HFD group (22.61g±1.10g). Neural tube HE staining showen that compared with the Control group, the neuronal maturity of the Mex3c group and the HFD group was reduced. Immunohistochemical staining showed that both fos and leptin were expressed on the nucleus, and LEPR was expressed on the cell membrane. Western blot experiments showed that compared with the Control group, the Mex3c group and the HFD group had low expression of fos protein (P<0.01), the Mex3c group had high expression of LEPR protein (P<0.01) and the HFD group had high expression of LEPR protein (P<0.01). Immunostaining experiments showed that nestin was expressed in nerve fibers, and PAX3 and H3K27me3 were both expressed in the nucleus. Western blooting experiment showed that compared with the Control group, the Mex3c group had high expression of nestin protein (P<0.01), PAX3 protein (P<0.01), H3K27me3 (P<0.01), and the HFD group had high expression of nestin protein (P<0.01). ) And PAX3 protein (P<0.01), H3K27me3 (P<0.01).ConclusionsMex3c regulates leptin and LEPR by enhancing the expression of fos mRNA to participate in the neural tube development process of offspring. The neural tube nestin, PAX3, and H3K27me3 of the offspring of Mex3c+/- mice and high-fat diet mice continue to be highly expressed. Mex3c+/- mice express low leptin, and high-fat diet mice highly express leptin; preliminary reveals the regulation of different energy states Leptin-LEPR is involved in the process of neurodevelopment. Mex3c mutant mice and mice on a high-fat diet lead to decreased neurodevelopmental maturity.


2018 ◽  
Vol 34 (5) ◽  
pp. 933-938 ◽  
Author(s):  
Emrah Kantarcioglu ◽  
Gokmen Kahilogullari ◽  
Murat Zaimoglu ◽  
Esin Ozlem Atmis ◽  
Elif Peker ◽  
...  

2020 ◽  
Author(s):  
Xinyue Li ◽  
Guangyu Ji ◽  
Juan Zhou ◽  
Jingyi Du ◽  
Xian Li ◽  
...  

Abstract Objective Early neural tube development in the embryo includes neural induction and self-renewal of neural stem cells (NSCs). The abnormal of neural tube development could lead to neural tube defects. The research on the mechanism of neural induction is the key to reveal the pathogenesis of the abnormal of neural tube. Though studies have confirmed a genetic component, the responsible mechanisms for the abnormal of neural tube are still largely unknown. Polycomb repressive complex 1 (PRC1) plays an important role in regulating early embryonic development, and has been sub-classified into six major complexes based on the presence of a Pcgf subunit. Pcgf1, as one of six Pcgf paralogs, is an important requirement in early embryonic brain development. Here, we intended to investigate the role and mechanism of Pcgf1 in early neural tube development of zebrafish embryos. Material and methods Morpholino (MO) antisense oligonucleotides were used to construct a Pcgf1 loss-of function zebrafish model. We analyzed the phenotype of zebrafish embryos and the expression of related genes in the process of neural induction by in situ hybridization, immunolabelling and RNA-sEq. The regulation of histone modifications on gene was detected by western blot and chromatin immunoprecipitation. Results In this study, we found that zebrafish embryos exhibited small head and reduced or even absence of telencephalon after inhibiting the expression of Pcgf1. Moreover, the neural induction process of zebrafish embryos was abnormal, and the subsequent NSCs self-renewal was inhibited under the inhibition of Pcgf1. RNA-seq and gene ontology (GO) analysis identified that the differentially expressed genes were enriched in many functional categories which related to the development phenotype. Finally, our results showed that Pcgf1 regulated the trimethylation of histone H3K27 in the Ngn1 and Otx2 promoter regions, and the levels of H3K4me3 at the promoters of Pou5f3 and Nanog. Conclusion Together, our data for the first time demonstrate that Pcgf1 plays an essential role in early neural induction phase through histone methylation in neural tube development. Our findings reveal a critical context-specific function for Pcgf1 in directing PRC1 to control cell fate.


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