Prenatal cocaine exposure increases mesoprefrontal dopamine neuron responsivity to mild stress.
Prenatal cocaine exposure increases mesoprefrontal dopamine neuron responsivity to mild stress.
复制标题
产前接触可卡因会增加中前额叶多巴胺神经元对轻度压力的反应性。
DOI：
10.1002/syn.1102
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Roth,RH
中科院分区：
文献类型：
--
作者：
Elsworth,JD;Morrow,BA;Roth,RH
母亲在怀孕期间使用可卡因的孩子似乎会增加某些神经行为缺陷的发生率。产前接触可卡因的啮齿动物模型模仿了后代的这些缺陷，但行为异常的生化基础尚不清楚。我们已经能够在产前可卡因暴露的大鼠静脉注射模型中重现短期记忆缺陷，并且由于短期记忆依赖于支配内侧前额叶皮层的多巴胺神经元的功能，我们假设产前可卡因会诱导该通路的调节功能障碍。在这里，我们报告，轻微的足部电击应激优先激活中前额叶多巴胺系统，导致在子宫内接触可卡因的青少年（出生后第35-37天）大鼠的腹内侧前额叶皮层多巴胺周转增加，这表明支配该区域的多巴胺神经元在这些大鼠中反应过度。因此，这种生化改变可能是胎儿发育期间接触可卡因的后代表现出的一些认知缺陷的核心。突触 42:80–83, 2001。© 2001 Wiley-Liss, Inc.
Children whose mothers used cocaine during pregnancy appear to have an increased incidence of certain neurobehavioral deficits. Rodent models of prenatal cocaine exposure have mimicked these deficits in the offspring, yet the biochemical basis of the behavioral abnormalities is unknown. We have been able to reproduce short‐term memory deficits in our rat intravenous model of prenatal cocaine exposure, and as short‐term memory is dependent on the function of dopamine neurons innervating the medial prefrontal cortex, we hypothesized that prenatal cocaine induces a dysfunction in the regulation of this pathway. Here we report that mild footshock stress, which preferentially activates the mesoprefrontal dopamine system, leads to an enhanced increase in dopamine turnover in the ventromedial prefrontal cortex of adolescent (postnatal day 35–37) rats exposed to cocaine in utero, suggesting that the dopamine neurons innervating this region are hyperresponsive in these rats. Thus, this biochemical alteration may be central to some of the cognitive deficits exhibited by offspring that were exposed to cocaine during fetal development. Synapse 42:80–83, 2001. © 2001 Wiley‐Liss, Inc.