ABSTRACT
Objective In order to explore the mechanizms of thymosin action on hypothalamus. Methods RT-PCR and in situ hybridization histochemistry (ISHH)were used. Results The expression of prothymosin ?1-mRNA was detected in preoptic area of hy- pothalamus by using RT-PCR technique. The results of ISHH showed that prothymosin ?1-mRNA was expressed in the preoptic mag- nocellular nucleus, suprachiasmatic nuclei and paraventricular nuclei of hypothalamus. In addition, the positive signal of prothymosin ?1- mRNA was also observed both in the microglicyte near the third ventricle and in medium to small sized pyramidal cells in cerebral cor- tex. Conclusion Prothymosin ?1 is produced in preoptic area of the hypothalamus by means of paracrine, which indicates that prothy- mosin ?1 participates in the regulation of hypothalamic function.
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AIM To develop a murine model for investigating the effects of prenatal cocaine exposure on the development of fetal nerve system. METHODS A nutritionally paired control group of dams injected with saline and pair fed with the COC dams were set up. Another two groups were COC groups injected with cocaine HCl and SAL group administrated with saline. After injection twice daily during gestation days 8～17,mice were decapitated on E17 and blood and brain samples were collected for pharmacological analysis and neurotransmitter analysis by HPLC.RESULTS Pharmacological analysis revealed that cocaine was found in maternal and fetal plasma at 15 min following ip administration to embryonic day E17 pregnant mice. Though COC dams and SPF dams had the same feeding condition, compared with the latter, the former had higher maternal concentrations of DA and 5 HT, lower fetal weight, brain weight, striatum weight and higher concentrations of DA and 5 HT in striatum, P
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AIM To investigate the effects of in utero cocaine exposure on the fetal development, when fetuses were exposed to equal total dose but different dose and timing. METHODS Pregnant dams were randomly separated into three groups: SAL, COC20 and COC40. On E17, recorded body weight, brain weight and striatum weight of all groups, and examined the concentrations of DA and 5 HT in fetal striatum by HPLC. RESULTS Body weight of SAL, COC40, COC20 groups decreased progressively in turns. Brain weight of COC20 group and COC40 group was lower than that of SAL. Only the brain/body ratio of COC40 was decreased ( P
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Objective To study the effects of prenatal cocaine exposure on the development of offspring's brains by building a murine model. Methods We weighted the body weight and brain weight of offspring on P10 from COC and SAL groups and observed the development of neuron and astrocyte in cerebral cortex by toluidine blue staining and immunohistochemistry. Results The brain weight and body weight from COC were both reduced on P10 compared with SAL group.We discovered prenatal cocaine exposure induced polarity disorder and dysplasia of neuron in cerebral cortex;the number of the astrocytes in corpus callosum and hippocampus regions decreased.Conclusion\ Pregnatal cocaine exposure can result in abnormal development of cerebral cortex of offsprings which may play an important role on cocaine induced abnormal behavior.\;[