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Cocaine-induced changes in the expression of apoptosis-related genes in the fetal mouse cerebral wall.可卡因诱导的胎鼠脑壁中凋亡相关基因表达的变化。
Neurotoxicol Teratol. 2005 Jan-Feb;27(1):3-14. doi: 10.1016/j.ntt.2004.08.004.
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Comparison of plasma cocaine levels during a "binge" pattern of cocaine administration in male and female rhesus monkeys.
Psychopharmacology (Berl). 2002 Oct;164(1):19-26. doi: 10.1007/s00213-002-1188-x. Epub 2002 Aug 9.
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Indicators of cocaine exposure and preterm birth.可卡因暴露和早产的指标。
Obstet Gynecol. 2002 Mar;99(3):458-65. doi: 10.1016/s0029-7844(01)01735-5.
4
Brain lesions induced by chronic cocaine administration to rats.长期给大鼠注射可卡因所诱发的脑部损伤。
Prog Neuropsychopharmacol Biol Psychiatry. 2002 Jan;26(1):59-63. doi: 10.1016/s0278-5846(01)00229-9.
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Primates exposed to cocaine in utero display reduced density and number of cerebral cortical neurons.在子宫内接触可卡因的灵长类动物,其大脑皮质神经元的密度和数量会降低。
J Comp Neurol. 2001 Jul 2;435(3):263-75. doi: 10.1002/cne.1028.
6
Regional differences in cell loss associated with binge-like alcohol exposure during the first two trimesters equivalent in the rat.在大鼠妊娠前两个月,与暴饮暴食样酒精暴露相关的细胞损失存在区域差异。
Alcohol. 2001 Jan;23(1):49-57. doi: 10.1016/s0741-8329(00)00133-6.
7
Cocaine induces cell death within the primate fetal cerebral wall.可卡因会导致灵长类胎儿脑壁内的细胞死亡。
Neuropathol Appl Neurobiol. 1999 Dec;25(6):504-12. doi: 10.1046/j.1365-2990.1999.00211.x.
8
Hippocampal dysplasia in rats exposed to cocaine in utero.子宫内接触可卡因的大鼠海马发育异常。
Brain Res Dev Brain Res. 1999 Nov 18;117(2):213-7. doi: 10.1016/s0165-3806(99)00106-6.
9
Brain damage and hypoxia in an ovine fetal chronic cocaine model.绵羊胎儿慢性可卡因模型中的脑损伤与缺氧
Eur J Obstet Gynecol Reprod Biol. 1999 Sep;86(1):15-22. doi: 10.1016/s0301-2115(99)00036-6.
10
Motor development of cocaine-exposed children at age two years.可卡因暴露儿童两岁时的运动发育情况。
Pediatrics. 1999 Jan;103(1):86-92. doi: 10.1542/peds.103.1.86.

在妊娠后期和出生后早期接触可卡因的大鼠在后期生活中表现出海马锥体细胞和颗粒细胞的缺陷。

Rats exposed to cocaine during late gestation and early postnatal life show deficits in hippocampal pyramidal and granule cells in later life.

作者信息

Ismail Zul Izhar Mohd, Bedi Kuldip S

机构信息

School of Biomedical Sciences, University of Queensland, St Lucia, Australia.

出版信息

J Anat. 2007 Jun;210(6):749-60. doi: 10.1111/j.1469-7580.2007.00735.x.

DOI:10.1111/j.1469-7580.2007.00735.x
PMID:17523939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2375763/
Abstract

In humans, the offspring of maternal cocaine misusers are known to have subtle cognitive and motor impairments in later life. It was therefore hypothesized that such exposure in animals would also affect the morphological structure of the brain. This possibility was investigated by exposing rats to cocaine between embryonic day 15 and postnatal day 6. Samples of the cocaine-exposed and control rats were killed for examination at 22 and 150 postnatal days of age. Stereological procedures (the Cavalieri principle together with the physical disector method) were utilized to estimate the total number of pyramidal and granule cells in defined regions of the hippocampal formation. At 22 days of age, the control offspring had about 373 000 pyramidal cells whereas the cocaine-treated animals only had about 310,000 cells in the CA1 + CA2 + CA3 region. By 150 days of age the values were about 396,000 and 348,000, respectively. The differences between age-matched groups were statistically significant. There were about 626,000 and 687,000 dentate gyrus granule cells in the 22-day-old control and cocaine-treated groups, respectively. By postnatal day 150 the control rats had about 832,000 granule cells whilst the cocaine-treated rats had about 693,000. There was a significant main effect of age as well as group-age interaction in this measure. These results show that even moderate exposure to cocaine during the late gestation and early postnatal period in rats is a potent teratogen and can markedly influence the development of neurons in the hippocampal formation.

摘要

众所周知,人类中母亲滥用可卡因的后代在日后生活中会出现细微的认知和运动障碍。因此,有人提出假说,认为动物受到此类影响也会改变大脑的形态结构。为了验证这一可能性,研究人员在胚胎第15天至出生后第6天期间让大鼠接触可卡因。在出生后第22天和第150天,处死暴露于可卡因的大鼠和对照大鼠并进行检查。采用体视学方法(卡瓦列里原理结合物理分割器法)来估计海马结构特定区域内锥体细胞和颗粒细胞的总数。在出生后第22天,对照后代在CA1 + CA2 + CA3区域约有373,000个锥体细胞,而经可卡因处理的动物只有约310,000个细胞。到出生后第150天,相应数值分别约为396,000和348,000。年龄匹配组之间的差异具有统计学意义。在出生后第22天,对照组和经可卡因处理组的齿状回颗粒细胞分别约有626,000个和687,000个。到出生后第150天,对照大鼠约有832,000个颗粒细胞,而经可卡因处理的大鼠约有693,000个。在这一指标上,年龄的主效应以及组 - 年龄交互作用均显著。这些结果表明,即使在大鼠妊娠后期和出生后早期适度接触可卡因,也是一种强效致畸剂,会显著影响海马结构中神经元的发育。