Jablonski S A, Stanton M E
Psychology Department, University of Delaware, Wolf Hall 108, Newark, DE 19716, USA.
Psychology Department, University of Delaware, Wolf Hall 108, Newark, DE 19716, USA.
Alcohol. 2014 Feb;48(1):35-42. doi: 10.1016/j.alcohol.2013.11.002. Epub 2013 Dec 2.
Alcohol exposure on postnatal days (PND) 4-9 in the rat adversely affects hippocampal anatomy and function and impairs performance on a variety of hippocampus-dependent tasks. Exposure during this developmental window reveals a linear relationship between alcohol dose and spatial learning impairment in the context preexposure facilitation effect (CPFE), a hippocampus-dependent variant of contextual fear conditioning. The purpose of the current report was to examine the effect of a range of alcohol doses administered during a narrower window, PND7-9, than previously reported (Experiment 1) and to begin to determine which memory processes involved in this task are impaired by developmental alcohol exposure (Experiment 2). In Experiment 1, rats pups received a single day binge alcohol dose of either 2.75, 4.00, 5.25 g/kg/day or were sham-intubated (SI) from PND7-9. Conditioned freezing during the test day was evident in all dosing groups, except for Group 5.25 g, indicating no graded dose-related behavioral deficits with alcohol exposure limited to PND7-9. In Experiment 2, rat pups were exposed to the highest effective dose from Experiment 1 (5.25 g/kg/day) or were sham intubated over PND7-9. During training, rats remained in the conditioning context for 5-min following immediate shock delivery. During this test of post-shock freezing, both SI and alcohol-exposed rats given prior exposure to the conditioning context showed comparable freezing levels. Since alcohol-exposed rats showed normal post-shock freezing, deficits by these rats on the test day likely reflect a failure to consolidate or retrieve a context-shock association, rather than a deficit in hippocampal conjunctive processes (consolidation, pattern completion) that occur prior to shock on the training day. These findings illustrate the value of the CPFE for characterizing the separable memory processes that are impaired by neonatal alcohol exposure in this task.
大鼠出生后第4至9天暴露于酒精会对海马体的解剖结构和功能产生不利影响，并损害其在各种依赖海马体的任务中的表现。在这个发育窗口期的暴露揭示了在情境预暴露促进效应（CPFE，一种依赖海马体的情境恐惧条件反射变体）中酒精剂量与空间学习障碍之间的线性关系。本报告的目的是研究在比先前报告更窄的窗口期（出生后第7至9天）给予一系列酒精剂量的影响（实验1），并开始确定在这项任务中涉及的哪些记忆过程会因发育期间暴露于酒精而受损（实验2）。在实验1中，幼鼠从出生后第7至9天接受单日暴饮酒精剂量，分别为2.75、4.00、5.25克/千克/天，或进行假插管（SI）。除了5.25克组外，所有给药组在测试日的条件性僵立都很明显，这表明仅限于出生后第7至9天暴露于酒精时，没有与剂量相关的行为缺陷分级。在实验2中，幼鼠在出生后第7至9天暴露于实验1中的最高有效剂量（5.25克/千克/天）或进行假插管。在训练期间，大鼠在立即电击后在条件化情境中停留5分钟。在这个电击后僵立测试中，先前暴露于条件化情境的SI组和酒精暴露组大鼠表现出相当的僵立水平。由于酒精暴露组大鼠电击后僵立正常，这些大鼠在测试日的缺陷可能反映了巩固或提取情境-电击关联的失败，而不是训练日电击前发生的海马体联合过程（巩固、模式完成）的缺陷。这些发现说明了CPFE在表征此任务中因新生儿酒精暴露而受损的可分离记忆过程方面的价值。
