Dose-dependent effects of acute in vivo ethanol exposure on extracellular glutamate concentration in the cerebral cortex of the near-term fetal sheep.
Dose-dependent effects of acute in vivo ethanol exposure on extracellular glutamate concentration in the cerebral cortex of the near-term fetal sheep.
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体内急性乙醇暴露对近期胎羊大脑皮层细胞外谷氨酸浓度的剂量依赖性影响。
DOI：
10.1111/j.1530-0277.1995.tb01006.x
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Brien,JF
中科院分区：
文献类型：
--
作者：
Reynolds,JD;Penning,DH;Dexter,F;Atkins,B;Hrdy,J;Poduska,D;Chestnut,DH;Brien,JF
大脑皮层是乙醇致畸作用的靶部位，L-谷氨酸是一种主要的兴奋性神经递质，在脑发育中起着重要的神经营养作用。已经提出谷氨酸神经元系统的最佳功能是正常脑发育所必需的;过度激活可能导致兴奋性毒性诱导的神经元损伤，而激活不足可能延迟/限制脑发育。本研究的目的是检验急性体内乙醇暴露改变胎儿大脑皮质中基础谷氨酸释放的假设。实验方法涉及测量胎儿皮质细胞外谷氨酸浓度使用在体内微透析技术。对近足月胎羊进行长期仪器化处理，将微透析探针放置在脑旁皮质中。在妊娠124 ± 3天时，测定了母体静脉输注2 g或4 g乙醇/kg母体体重或等量生理盐水（在5小时内以4个等分剂量给药）对胎仔大脑皮质细胞外谷氨酸浓度的影响。在研究期间，三种治疗方案均未导致胎儿或母体死亡。胎仔大脑皮层细胞外谷氨酸浓度呈乙醇剂量依赖性增加，p= 0.005。这种增加是阵发性的，与胎仔血液乙醇浓度没有直接关系。鉴于谷氨酸在神经元发育中的作用，乙醇诱导的谷氨酸释放明显增加可能在涉及大脑皮层的乙醇致畸作用的发病机制中很重要。
The cerebral cortex is a target site of ethanol teratogenesis.l‐Glutamate is a major excitatory neurotransmitter that plays an important neurotrophic role in brain development. It has been proposed that optimal function of the glutamate neuronal system is required for normal brain development; overactivation could lead to excitotoxic‐induced neuronal injury, whereas underactivation could delay/restrict brain development. The objective of this study was to test the hypothesis that acute in vivo ethanol exposure alters basal glutamate release in the fetal cerebral cortex. The experimental approach involved measuring fetal cortical extracellular glutamate concentration using the technique of in vivo microdialysis. Near‐term fetal sheep were chronically instrumented with a microdialysis probe placed in the parasagittal cortex. At 124 ± 3 days of gestation, the effects of maternal intravenous infusion of 2 g or 4 g ethanol/kg maternal body weight or an equivalent volume of saline, given as four equally divided doses over 5 hr, on fetal cerebral cortical extracellular glutamate concentration were determined. None of the three treatment regimens produced fetal or maternal demise during the time course of the study. There was an ethanol dose‐dependent increase,p= 0.005, in extracellular glutamate concentration in the fetal cerebral cortex. This increase was paroxysmal in nature and was not directly related to the fetal blood ethanol concentration. In view of the proposed role for glutamate in neuronal development, this apparent ethanol‐induced increase in glutamate release may be important in the pathogenesis of ethanol teratogenesis involving the cerebral cortex.
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影响因子：
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DOI：
--
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