Electrophysiological characterization of cerebellar neurons from adult rats exposed to ethanol during development
Electrophysiological characterization of cerebellar neurons from adult rats exposed to ethanol during development
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DOI：
10.1111/j.1530-0277.1998.tb03713.x
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发表时间：
1998-08-01
影响因子：
3.2
通讯作者：
Palmer, MR
中科院分区：
文献类型：
--
作者：
Bäckman, C;West, JR;Palmer, MR
本研究的目的是研究暴露于乙醇（ROH）的成熟大鼠小脑神经元在出生后4至10天（相当于人类妊娠晚期）的自发活动。将新生大鼠植入胃饲管，从出生后第4 ~ 10天开始用两种不同的饲料进行人工饲养。试验组给予4.5 g/kg/天的牛奶溶液ROH。对照组接受类似的喂养，用等热量补充剂代替EtOH。在无etoh饲养期后进行电生理评估。尽管与对照组相比，初生暴露于EtOH的动物小脑蚓部的第IX小叶和第X小叶在形态学上显得更小，但成年大鼠浦肯野细胞和高尔基中间神经元的细胞外记录显示，对照组和暴露于EtOH的动物在自发活动或放电模式上没有差异。同样，平行通路刺激引起的浦肯野神经元活动的兴奋和抑制不受发育性EtOH暴露的影响。然而，我们确实观察到，在新生儿暴露于EtOH的组中，产生复杂尖峰爆发的浦肯野神经元比例显著下降。这些数据表明，虽然较少的浦肯野神经元可能在大脑发育的关键时期存活下来，但那些存活下来的神经元似乎功能正常。观察到的复杂尖峰产生的异常可能是由于EtOH对下橄榄发育中的神经元的影响，导致攀爬纤维产生，导致浦肯野神经元的这种爆裂模式。
The purpose of this study was to investigate the spontaneous activity of mature rat cerebellar neurons that had been exposed to ethanol (ROH) during postnatal days 4 to 10, which corresponds to the third trimester in humans. Newborn Sprague-Dawley rats were implanted with gastric feeding tubes and were artificially reared from postnatal days 4 to 10 with two different diets. The experimental group received 4.5 g/kg/day of ROH delivered in a milk solution. Controls received similar feeding with an isocaloric supplement replacing the EtOH. Electrophysiological evaluations were performed after an EtOH-free rearing period. Although lobules IX and X of the cerebellar vermis appeared morphologically smaller in the animals neonatally exposed to EtOH, compared with controls, extracellular recordings from both Purkinje cells and Golgi interneurons in adult rats showed no differences in spontaneous activity or firing pattern between the control and EtOH-exposed animals. Similarly, excitations and inhibitions of Purkinje neuron activity evoked by parallel pathway stimulation appeared unaffected by the developmental EtOH exposure. However, we did observe a significant decrease in the proportion of Purkinje neurons generating complex spike bursts in the group exposed to EtOH neonatally. These data suggest that, although fewer Purkinje neurons may survive the brain growth spurt if exposed to EtOH during this critical period of development, those that do survive appear to function normally. The observed abnormality in complex spike production may result from EtOH effects on developing neurons in the inferior olive that give rise to the climbing fibers that cause this bursting pattern in Purkinje neurons.