Deficits in trace fear conditioning in a rat model of fetal alcohol exposure: dose-response and timing effects.
Deficits in trace fear conditioning in a rat model of fetal alcohol exposure: dose-response and timing effects.
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DOI：
10.1016/j.alcohol.2009.08.004
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发表时间：
2009-09
期刊：
影响因子：
--
通讯作者：
Torok EJ
中科院分区：
文献类型：
--
作者：
Hunt PS;Jacobson SE;Torok EJ
在人类中，产前酒精暴露会导致几种类型的学习和记忆的严重损害，包括陈述性记忆和空间记忆。动物模型有助于证实许多观察到的影响是酒精暴露的结果，而不是继发于母亲营养不良或不利的家庭环境。报告称，在新生期（出生后[PD] 4-9天）暴露于乙醇的大鼠在青少年时期接受训练时表现出微量恐惧条件反射受损，但延迟恐惧条件反射未受影响。本系列的三个实验代表了一个更详细的分析乙醇诱导的赤字在跟踪条件。在实验1中，给予新生儿的乙醇剂量不同（3.0、4.0或5.0 g/kg/天）。痕量条件反射呈剂量依赖性降低，在最高剂量处理的动物中观察到最差的性能。在实验2中，人们发现，从新生儿乙醇暴露导致的跟踪条件的损害是依赖于用于培训的跟踪间隔的持续时间;学习少是明显的乙醇暴露的动物训练较长的跟踪间隔的持续时间。这些结果证实了延迟依赖性记忆缺陷的其他报告。最后，实验3确定，乙醇暴露限于新生儿期的前半部分（PD 4-6）比暴露于后半部分（PD 7-9）对后期痕迹条件反射更有害。这些结果支持了这一假设，即早期乙醇暴露导致的痕量条件反射损伤是由于药物对发育中海马的致畸作用，因为这些发现与在离散海马病变动物中观察到的结果相似。在大脑生长突增期暴露于乙醇的动物中，延迟和微量恐惧条件反射性能之间的比较提供了一个模型系统，用于研究胎儿酒精谱系障碍的选择性学习障碍和可能的治疗方法。
In humans, prenatal alcohol exposure can result in significant impairments in several types of learning and memory, including declarative and spatial memory. Animal models have been useful for confirming that many of the observed effects are the result of alcohol exposure, and not secondary to poor maternal nutrition or adverse home environments. reported that rats exposed to ethanol during the neonatal period (postnatal days [PD] 4–9) exhibited impaired trace fear conditioning when trained as adolescents, but were unaffected in delay fear conditioning. The present series of three experiments represent a more detailed analysis of ethanol-induced deficits in trace conditioning. In Experiment 1 the dose of ethanol given to neonates was varied (3.0, 4.0 or 5.0 g/kg/day). There was a dose-dependent reduction in trace conditioning, with the poorest performance observed in animals treated with the highest dose. In Experiment 2 it was found that the impairment in trace conditioning resulting from neonatal ethanol exposure was dependent on the duration of the trace interval used for training; less learning was evident in ethanol-exposed animals trained with longer trace interval durations. These results confirm other reports of delay-dependent memory deficits. Finally, Experiment 3 determined that ethanol exposure limited to the first half of the neonatal period (PD 4–6) was more detrimental to later trace conditioning than exposure during the second half (PD 7–9). These results support the hypothesis that trace conditioning impairments resulting from early ethanol exposure are due to the drug’s teratogenic effects on the developing hippocampus, as the findings parallel those observed in animals with discrete hippocampal lesions. Comparisons between delay and trace fear conditioning performance in animals exposed to ethanol during the brain growth spurt provide a model system to study both selective learning impairments and possible treatment approaches for humans with fetal alcohol spectrum disorders.
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影响因子：
2.7
作者：
Eichenbaum, H
通讯作者：
Eichenbaum, H
DOI：
10.1097/00000374-200003000-00007
发表时间：
2000-03-01
影响因子：
3.2
作者：
Girard, TA;Xing, HC;Wainwright, PE
通讯作者：
Wainwright, PE
影响因子：
5.1
作者：
CLARREN, SK;ASTLEY, SJ;SPELLMAN, D
通讯作者：
SPELLMAN, D
影响因子：
3.4
作者：
Herrera-Morales, Wendy;Mar, Ivonne;Bermudez-Rattoni, Federico
通讯作者：
Bermudez-Rattoni, Federico
影响因子：
2.5
作者：
DOBBING, J;SANDS, J
通讯作者：
SANDS, J