Taste aversion learning in preweanling rats exposed to alcohol prenatally.
Taste aversion learning in preweanling rats exposed to alcohol prenatally.
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产前接触酒精的断奶前大鼠的味觉厌恶学习。
DOI：
10.1002/tera.1420290303
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Chen,JS
中科院分区：
文献类型：
--
作者：
Riley,EP;Barron,S;Driscoll,CD;Chen,JS
在未断奶的大鼠幼崽中，研究了产前酒精暴露对条件性味觉厌恶发展的影响。从妊娠第6天到第20天，这些幼崽的母亲被喂食含有35%或0%乙醇衍生卡路里（EDC）的等热量液体饲料。采用配对饲养程序，并包括一个随机实验室饲料对照组。在5日龄、10日龄或15日龄时，幼犬通过植入口腔的导管注入糖精溶液。然后，每组一半幼鼠注射氯化锂（LiCl）作为中毒剂，另一半幼鼠注射氯化钠（NaCl）作为对照。随后对动物进行了条件反射性厌恶糖精溶液的测试。在15日龄时，LiCl中毒组的所有幼崽都表现出对糖精溶液的条件性味觉厌恶，但这种厌恶程度在酒精暴露的幼崽中较低。在10天大的时候，狗狗学会了厌恶味道，尽管不像15天大的狗狗那样强烈，但所有产前治疗组的狗狗似乎都学得很好。在5日龄时，味觉厌恶学习有边缘性支持。同样，它与产前治疗没有相互作用。从海马发育改变的角度讨论了酒精暴露后代相对于对照组表现出的味觉厌恶学习的个体差异。
The effects of prenatal alcohol exposure on the development of a conditioned taste aversion were examined in preweanling rat pups. Mothers of these pups were fed isocaloric liquid diets containing either 35 or 0% ethanolderived calories (EDC) from gestation days 6 through 20. A pair‐feeding procedure was employed, and an ad lib lab chow control group was also included. At 5, 10, or 15 days of age, pups were infused with a saccharin solution through a cannula implanted in the oral cavity. Half of the pups in each group were then injected with lithium chloride (LiCl), which served as the poisoning agent, and the other half with sodium chloride (NaCl) as a control. Animals were subsequently tested for a conditioned aversion to the saccharin solution. At 15 days of age, all of the pups in the LiCl‐poisoned group demonstrated a conditioned taste aversion to the saccharin solution, but the degree of this aversion was less in alcohol‐exposed offspring. At 10 days of age, a taste aversion was learned, although it was not as strong as that shown by 15‐day‐old pups, and it appeared to be learned equally well by all of the prenatal treatment groups. At 5 days of age, there was marginal support for taste aversion learning. Again, it did not interact with prenatal treatment. The ontogenic differences in taste aversion learning exhibited by alcohol‐exposed offspring relative to controls are discussed in terms of altered hippocampal development.