盡管20世紀80年代有關(guān)“可卡嬰”（備注1）的報道被嚴重夸大,，但母體懷孕階段接觸可卡因確實可以引起后代輕微的先天性功能障礙——注意力缺陷，學(xué)習(xí)障礙和情感問題等,。
美國范德比大學(xué)肯尼迪人類發(fā)展研究中心(*)的研究者們在產(chǎn)前可卡因接觸對胎兒行為,、神經(jīng)影響方面有著更為深入的理解。在最新發(fā)表在《Journal of Neuroscience》雜志上的文章中,，Gregg Stanwood和Pat Levitt通過對兔子的研究,，發(fā)現(xiàn)產(chǎn)前可卡因接觸會引起某些腦細胞多巴胺受體的長期移位，從而妨礙了它們正常功能的行使,。
更為具體地說,，研究者在兔子模型中發(fā)現(xiàn)多巴胺D1受體（dopamine D1 receptor）盡管在神經(jīng)元中的表達總量沒有明顯變化，但蛋白分布卻發(fā)生了顯著變化：由細胞表面跑進了細胞內(nèi)部,。
如果這個在人類中也有同樣的規(guī)律,，“這將有助于我們?nèi)椭欣щy的孩子。”因為可卡因接觸似乎可以改變D1受體的分布，Stanwood建議研究者開發(fā)出一種方法讓受體“迷途知返”,。
“現(xiàn)在還沒有學(xué)者得到人相關(guān)的數(shù)據(jù),，” Stanwood說道，“接下去的研究將會非常關(guān)鍵,。”
英文詞匯：
*Vanderbilt Kennedy Center for Research on Human Development
備注1：crack baby,；患有某種先天性功能不全的嬰兒,因孕婦吸食可卡因而感染的。
英文原文：
Cocaine use during pregnancy has lasting cellular effects
A new study has found that though the "crack baby" hysteria of the 1980s was greatly exaggerated, using cocaine during pregnancy can nonetheless cause subtle but disabling cognitive impairments in kids.
These impairments include attention deficits, learning disabilities and emotional problems.
The study was conducted by researchers at the Vanderbilt Kennedy Center for Research on Human Development.
Researchers Gregg Stanwood, Ph.D., and Pat Levitt, Ph.D., in a study on rabbits, found that prenatal cocaine exposure causes a long lasting displacement of dopamine receptors in certain brain cells, which alters their ability to function normally.
Dr Stanwood said that though the "crack baby" hysteria was "sort of overblown", using high levels of cocaine - usually coupled with the abuse of other drugs - can lead to premature labour, preterm birth and low birth weight.
"The hysteria surrounding the 'crack baby' was sort of overblown," said Stanwood, research assistant professor of Pharmacology and lead author on the study.
He added that even though children of women who have used low recreational doses of cocaine seem to be "normal" at birth, they tend to develop deficits in their cognitive and emotional development as they grow older.
"But in women who have abused relatively low recreational doses of cocaine, it is actually very hard to distinguish those children at birth from children born to anyone else. However, as those children age, they do develop deficits in their cognitive and emotional development," he said.
These children often exhibit attention and arousal problems, similar to children with attention deficit hyperactivity disorder (ADHD). However, the standard treatments for ADHD -- Ritalin and other stimulants -- are not always effective in these children.
In a previous study, the researchers had found that exposure to low levels of intravenous cocaine during a very short window of time during gestation - equivalent to the late first trimester and early second trimester in humans - caused specific alterations in brain circuits that use the neurotransmitter dopamine that is involved in regulating the formation of cortical circuitry.
Additionally, these cocaine-exposed offspring showed attention problems as well as insensitivity to stimulants like amphetamine, suggesting that cocaine exposure had altered the development of the dopamine pathways in the brain.
"In collaboration with Dr. Eitan Friedman of the City University of New York, we had previously shown a decrease in signalling of a particular receptor protein, the dopamine D1 receptor. We know that this receptor is involved in regulating the formation of cortical circuitry. It's also involved in the behavioural effects of amphetamines and cocaine," Dr Stanwood.
As a part of the present study, Dr Stanwood examined the levels of D1 receptor in brain cells taken from "teenage" rabbits that were exposed to cocaine during that short, sensitive prenatal period, and found that though cocaine exposure did not alter the total amount of D1 receptor produced in the brain, however, there was a dramatic alteration in the location of the protein within the cell.
D1 receptors are normally found at the cell surface, but neurons from the cocaine-exposed animals showed the receptor was predominantly sequestered inside the cells.
The effect, which "appears permanent" the researchers state, implies that cocaine exposure during a brief, sensitive period of neural development can lead to long-lasting effects at the cellular level.
This change also altered the growth of neuronal processes, suggesting that the altered D1 receptor trafficking may underlie the changes in neuronal architecture and behaviour.
The researchers insisted that though this effect has not yet been assessed in cocaine-exposed children, the findings gives them a place to start looking.
"Neither we nor anyone else has yet identified whether this mechanism occurs in the human population so that is a critical next step," Stanwood said.
The study is published in a recent issue of the Journal of Neuroscience.
