• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

小鼠16三体胚胎脑发育的形态学和神经化学研究。

Morphologic and neurochemical studies of embryonic brain development in murine trisomy 16.

作者信息

Singer H S, Tiemeyer M, Hedreen J C, Gearhart J, Coyle J T

出版信息

Brain Res. 1984 Aug;317(2):155-66. doi: 10.1016/0165-3806(84)90093-2.

DOI:10.1016/0165-3806(84)90093-2
PMID:6148129
Abstract

Telencephalic and diencephalic/brainstem regions from embryonic trisomy-16 mice (Ts16) between gestational days 15-18 were analyzed for alterations of morphologic and neurochemical parameters and compared to phenotypically normal littermates. Mean trisomic wet weights from both regions were significantly diminished (greater than 20%) and total protein content was reduced. Ratios of the thickness of the ventricular (germinal) zone to the thickness of the whole cortex were increased, suggesting a delay in neuronal differentiation. Pre- and postsynaptic markers for GABAergic, cholinergic, catecholaminergic and serotonergic transmitter systems were compared. A significant impairment of the trisomic brain catecholaminergic and serotonergic system development was observed, based upon regional reductions in norepinephrine, dopamine and serotonin content. Choline acetyltransferase activity in the diencephalon/brainstem was reduced by 21-26% in contrast to normal levels within the cerebral hemispheres. Presynaptic GABAergic markers were not affected in the Ts16 embryos. It is concluded that although a genetic imbalance involving chromosome 16 in the mouse embryo produces a delay in neurogenesis, it has a more selective effect on the catecholaminergic, serotonergic and cholinergic systems than on GABAergic neurons.

摘要

对妊娠第15 - 18天的胚胎16三体小鼠(Ts16)的端脑和间脑/脑干区域进行分析,以观察形态学和神经化学参数的变化,并与表型正常的同窝小鼠进行比较。两个区域的三体平均湿重均显著降低(超过20%),总蛋白含量减少。脑室(生发)区厚度与整个皮质厚度的比值增加,提示神经元分化延迟。比较了γ-氨基丁酸能、胆碱能、儿茶酚胺能和5-羟色胺能递质系统的突触前和突触后标志物。基于去甲肾上腺素、多巴胺和5-羟色胺含量的区域减少,观察到三体脑儿茶酚胺能和5-羟色胺能系统发育存在显著损害。与大脑半球内的正常水平相比,间脑/脑干中的胆碱乙酰转移酶活性降低了21 - 26%。Ts16胚胎中的突触前γ-氨基丁酸能标志物未受影响。得出的结论是,尽管小鼠胚胎中涉及16号染色体的基因失衡会导致神经发生延迟,但它对儿茶酚胺能、5-羟色胺能和胆碱能系统的影响比对γ-氨基丁酸能神经元的影响更具选择性。

相似文献

1
Morphologic and neurochemical studies of embryonic brain development in murine trisomy 16.小鼠16三体胚胎脑发育的形态学和神经化学研究。
Brain Res. 1984 Aug;317(2):155-66. doi: 10.1016/0165-3806(84)90093-2.
2
Neurochemical characterization of embryonic brain development in trisomy 19 (Ts19) mice: implications of selective deficits observed for abnormal neural development in aneuploidy.19三体(Ts19)小鼠胚胎脑发育的神经化学特征:非整倍体中观察到的选择性缺陷对异常神经发育的影响。
Dev Genet. 1987;8(4):267-79. doi: 10.1002/dvg.1020080409.
3
Neurochemical changes in murine trisomy 16: delay in cholinergic and catecholaminergic systems.小鼠16三体中的神经化学变化:胆碱能和儿茶酚胺能系统的延迟
J Neurochem. 1984 Aug;43(2):401-8. doi: 10.1111/j.1471-4159.1984.tb00915.x.
4
Selective retardation of the development of the basal forebrain cholinergic and pontine catecholaminergic nuclei in the brain of trisomy 16 mouse, an animal model of Down's syndrome.唐氏综合征动物模型——16三体小鼠大脑中基底前脑胆碱能和脑桥儿茶酚胺能核团发育的选择性迟缓
Brain Res Dev Brain Res. 1989 Dec 1;50(2):251-64. doi: 10.1016/0165-3806(89)90201-0.
5
Coexistence of cholinergic, catecholaminergic, serotonergic, and glutamatergic neurotransmitter markers in mouse clonal hybrid neurons derived from the septal region.
J Neurosci Res. 1992 Jun;32(2):127-37. doi: 10.1002/jnr.490320202.
6
Regional alteration of cholinergic function in central neurons of trisomy 16 mouse fetuses, an animal model of human trisomy 21 (Down syndrome).16三体小鼠胎儿中枢神经元胆碱能功能的区域改变,人类21三体(唐氏综合征)的动物模型。
Brain Res. 1994 Sep 26;658(1-2):27-32. doi: 10.1016/s0006-8993(09)90006-3.
7
Neurochemical substrates and neuroanatomical generators of the event-related P300.事件相关P300的神经化学底物和神经解剖学发生器
Neuropsychobiology. 1999;40(2):86-94. doi: 10.1159/000026603.
8
Consequences of trisomy 16 for mouse brain development: corticogenesis in a model of Down syndrome.16号染色体三体对小鼠大脑发育的影响:唐氏综合征模型中的皮质发生
J Neurosci. 1996 Oct 1;16(19):6175-82. doi: 10.1523/JNEUROSCI.16-19-06175.1996.
9
Regional levels of neurotransmitter markers in the pigeon telencephalon: a comparison with possibly homologous areas of the rat telencephalon.鸽子端脑内神经递质标志物的区域水平:与大鼠端脑可能的同源区域的比较。
J Neurochem. 1988 Jun;50(6):1731-7. doi: 10.1111/j.1471-4159.1988.tb02471.x.
10
Studies on the mechanism of wet dog shakes produced by carbachol in rats.卡巴胆碱诱发大鼠湿狗样抖动机制的研究。
Pharmacology. 1984;28(2):112-20. doi: 10.1159/000137951.

引用本文的文献

1
Altered development of dopaminergic neurons differentiated from stem cells from human exfoliated deciduous teeth of a patient with Down syndrome.唐氏综合征患者人乳牙干细胞分化的多巴胺能神经元发育异常。
BMC Neurol. 2018 Aug 31;18(1):132. doi: 10.1186/s12883-018-1140-2.
2
The power of comparative and developmental studies for mouse models of Down syndrome.唐氏综合征小鼠模型的比较与发育研究的作用
Mamm Genome. 2007 Jul;18(6-7):431-43. doi: 10.1007/s00335-007-9030-8. Epub 2007 Jul 26.
3
Somatostatin expression in TS16 mouse brain cultures.
生长抑素在TS16小鼠脑培养物中的表达。
J Mol Neurosci. 1998 Apr;10(2):99-111. doi: 10.1007/BF02737121.
4
Glutamate as a hippocampal neuron survival factor: an inherited defect in the trisomy 16 mouse.谷氨酸作为海马神经元存活因子:16三体小鼠的遗传缺陷。
Proc Natl Acad Sci U S A. 1995 Oct 10;92(21):9692-6. doi: 10.1073/pnas.92.21.9692.
5
Blastomere karyotyping and transfer of chromosomally selected embryos. Implications for the production of specific animal models and human prenatal diagnosis.
Hum Genet. 1988 Dec;80(4):333-6. doi: 10.1007/BF00273646.
6
Nerve growth factor corrects developmental impairments of basal forebrain cholinergic neurons in the trisomy 16 mouse.神经生长因子可纠正16三体小鼠基底前脑胆碱能神经元的发育障碍。
Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1793-7. doi: 10.1073/pnas.88.5.1793.
7
Dysregulation of gene expression in mouse trisomy 16, an animal model of Down syndrome.唐氏综合征动物模型——小鼠16三体中基因表达的失调。
EMBO J. 1992 Feb;11(2):619-27. doi: 10.1002/j.1460-2075.1992.tb05094.x.