Neonatal alcohol exposure impairs acquisition of eyeblink conditioned responses during discrimination learning and reversal in weanling rats
Neonatal alcohol exposure impairs acquisition of eyeblink conditioned responses during discrimination learning and reversal in weanling rats
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DOI：
10.1002/dev.20178
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发表时间：
2007-04-01
影响因子：
2.2
通讯作者：
Stanton, Mark E.
中科院分区：
文献类型：
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作者：
Brown, Kevin L.;Calizo, Lyngine H.;Stanton, Mark E.
对经典条件眨眼反应的辨别和逆转依赖于小脑-脑干与海马体的相互作用。在断奶和成年大鼠中，新生的“狂欢”酒精暴露于5g/kg/天或更多剂量的酒精已被证明损害了单线索眨眼条件作用。本研究将新生大鼠暴露于不同发育期(出生后4-9天或PND7-9天)的急性酒精插管，并从PND26-31开始对它们进行辨别性经典眨眼条件反射和反转实验。高剂量(5g/kg/天)的酒精在PND4-9期间暴露时，与对照组相比显著损害条件反射，但在PND7-9期间给予时，产生轻微的损害或没有损害。这些发现支持了之前的说法，即发育暴露时间在确定酒精对发育中的大脑的有害影响方面发挥着关键作用。从PND4-9递送的较低剂量的酒精(4g/kg/天)-低于先前显示的影响单线索眨眼条件反射的剂量-也造成了辨别任务的缺陷，提示在翻转过程中辨别学习和对CS+反应的获得可能是该模型中酒精诱导的脑损伤的特别敏感的行为指标。(C)2007年威利期刊公司。
Discrimination and reversal of the classically conditioned eyeblink response depends on cerebellar-brainstem interactions with the hippocampus. Neonatal "binge" exposure to alcohol at doses of 5 g/kg/day or more has been shown to impair single-cue eyeblink conditioning in both weanling and adult rats. The present study exposed neonatal rats to acute alcohol intubations across different developmental periods (postnatal day [PND] 4-9 or PND7-9) and tested them from PND26-31 on discriminative classical eyeblink conditioning and reversal. A high dose of alcohol (5 g/kg/day) dramatically impaired conditioning relative to controls when exposure occurred over PND4-9, but produced mild or no impairments when delivered over PND7-9. These findings support previous claims that developmental exposure period plays a critical role in determining the deleterious effects of alcohol on the developing brain. A lower dose of alcohol (4 g/kg/day) delivered from PND4-9-lower than has previously been shown to affect single-cue eyeblink conditioning-also produced deficits on the discrimination task, suggesting that discrimination learning and acquisition of responding to CS+ during reversal may be especially sensitive behavioral indicators of alcohol-induced brain damage in this rat model. (c) 2007 Wiley Periodicals, Inc.