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RISS 인기검색어
- 검색키워드
- 저자 : Druse, Mary J. (검색결과 4 건)
- 무료
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Kim, Jung-Ae,Druse, Mary J. 영남대학교 약품개발연구소 1997 영남대학교 약품개발연구소 연구업적집 Vol.7 No.-
Previous work in this laboratory demonstrated that in utero ethanol exposure is associated with abnormal development of the serotonergic system. Specific abnormalities included deficiencies of serotonin (5-HT) and its metabolites, and cortical 5-HT reuptake sites. The concentration of 5-HT_(LA) receptors was also altered. The serotonin deficit was detected in the fetal ethanol-exposed brain, at an age when 5-HT would normally function as an essential trophic factor. Thus, it was hypothesized that the early 5-HT ethanol-associated deficit of an essential trophic factor (e.g. 5-HT) could contribute to subsequent developmental abnormalities in serotonergic neurons. In the present investigation we used quantitative autoradiography (QAR) to more fully characterize the developmental abnormalities in 5-HT reuptake sites in developing offspring of ethanol-fed rats. In addition, we attempted to overcome the potential negative impact of the ethanol-associated deficit of fetal 5-HT, by administering a 5-HT₁_(A) agonist, buspirone, to pregnant rats. These investigations demonstrated that postnatal (PN) 19 and/or 35 day ethanol-exposed offspring had a significant decrease in [³H]citalopram binding to 5-HT reuptake sites in the frontal cortex, parietal cortex. lateral hypothalamous, substantia nigra, medial septum, and striatum. In contrast, [³H ]citalopram binding was increased in the dorsal raphe on PN5 and in the median raphe on PN19. No significant ethanol-associated changes were detected in the hippocampus CA3 region or in the amygdala. When [³H]citalopram binding was compared in the offspring of saline- and buspirone-treated dams, it appeared that maternal treatment with buspirone prevented or reersed most of the ehanol-associated developmental abnormalities in 5-HT reuptake sites. Buspirone prevented the decline in binding of [³H ]citalopram in the frontal cortex, lateral hypothalamus, substantia nigra and medial septum. Similary, buspirone treatment preented the ethanol-associated increase in binding in the dorsal and median raphe. Additional experiments are needed to elucidate the impact of maternal buspirone treatrment on the development of other neurotransmitter systems in offspring.
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Kim, Jung-Ae,Druse, Mary J. 영남대학교 약품개발연구소 1997 영남대학교 약품개발연구소 연구업적집 Vol.7 No.-
Prior research in this laboratory has shown that in utero ethanol exposure adversely affects the development of serotonergic neurons. The current study investigated the hypothesis that cortical astrocytes produce trophic factors which are essential for the development of the fetal precursors of serotonergic and other raphe neurons (e.g. rhombencephalic neurons), and that ethanol exposure impairs the production of these factors by astrocytes. The results of these experiments demonstrated that cultured cortical astrocytes produce trophic factors which are necessary for the development of rhombencephalic neurons. Conditioned media obtained from control astrocytes promoted both general neuronal development (increased cell number, cell survival, DNA content, protein content, and ncurite outgrowth) and serotonergic neuronal development (increased number of serotonin (5-HT) immunopositive cells and [³H]5-HT uptake). However, the conditioned media produced by ethanol-treated astrocytes (ECM) lacked essential neorotrophic factors. Neuronal cultures maintained in ECM had reduced DNA and neuronal survival, and altered neurite outgrowth, 5-HT immunopositive neurons and [³H]5-HT uptake were also decreased in ECM cultures. Thus, the damaging effects of in utero ethanol exposure on developing serotonergic neurons may be due to impaired production of astroglial neurotrophic factors.
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Kim, Jung-Ae,Gilespie, Roberta A.,Druse, Mary J. 영남대학교 약품개발연구소 1998 영남대학교 약품개발연구소 연구업적집 Vol.8 No.-
In utero ethanol exposure results in a decreased concentration of serotonin (5-HT) in brain regions containing the cell bodies of 5-HT neurons and their cortical projections. The concentration of 5-HT reuptake sites is also reduced in several brain areas. The present study extended prior work by evaluating the effects of chronic maternal ethanol consumption and maternal buspirone treatment on 5-HT_(1A) and 5-HT_(2A) receptors in mutiple brain areas of offspring. Receptors were quantitated early in postnatal development and at an age when the 5-HT networks are normally well-established. Because fetal 5-HT functions as an essential neurotrophic factor, these studies also determined whether treatment of pregnant rats with buspirone, a 5-HT_(1A) agonist, could overcome the effects of the fetal 5-HT deficit and prevent ethanol-associated receptor abnormalities. The results demonstrated that in utero ethanol exposure significantly alters the binding of 0.1 nM [³H]-8-hydroxy-dipropylaminotetralin to 5-HT_(1A) receptors in developing animals. Ethanol impaired the development of 5-HT_(1A) receptors in the frontal cortex, parietal cortex, and lateral septum; these receptors did not undergo the normal developmental increase between postnatal days 19 and 35. The dentate gyrus was also sensitive to the effects of in utero ethanol exposure. 5-HT_(1A) receptors were increased in this region at 19 days. Maternal buspirone treatment prevented the ethanol-associated abnormalities in 5-HT_(1A) receptors in the dentate gyrus, frontal cortex, and lateral septum. Neither maternal ethanol consumption nor buspirone treatment altered the binding of 2 nM [³H]ketanserin to 5-HT_(2A) receptors in the ventral dentate gyrus,dorsal raphe, parietal and frontal cortexes, striatum, substantis nigra, or nucleus accumbens.
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