Intermittent ethanol exposure in adolescent rats: dose-dependent impairments in trace conditioning.

Intermittent ethanol exposure in adolescent rats: dose-dependent impairments in trace conditioning.
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青春期大鼠间歇性乙醇暴露:微量调节的剂量依赖性损伤。

DOI:
10.1097/01.alc.0000147657.51745.a7
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发表时间:
2004
期刊:
Alcoholism, clinical and experimental research
影响因子:
--
通讯作者:
Hunt,PamelaS
Hunt,PamelaS
中科院分区:
--
文献类型:
--
作者:
Yttri,EricA;Burk,JoshuaA;Hunt,PamelaS

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背景:最近的研究表明,青少年的大脑可能特别容易受到乙醇诱导的毒性。与成年期相比,青春期酒精暴露对皮质边缘区域的损害更为严重。然而,青少年酒精暴露对认知的影响直到最近才开始被探索。方法:雄性和雌性大鼠于青春期(出生后28、30、32、34天)急性灌胃分别给予0、1.5、2.5、4.5 g/kg乙醇(20% v/v)。在PD 40,每个剂量组中一半的受试者被给予5对10秒闪烁光(CS;条件刺激),紧接着是轻微的足部刺激(US;非条件刺激),这一过程被称为延迟条件反射。另一半也被给予5组CS - US配对,但在CS偏移10秒后出现US,这一过程被称为痕量条件反射。所有受试者在24小时后进行CS诱导冷冻测试。结果:青少年酒精暴露对延迟条件反应没有影响,所有受试者都表现出相当水平的CS诱发冻结。微量条件实验对象的冷冻量与先前的乙醇剂量呈负相关。具体而言,在青春期暴露于2.5或4.5 g/kg会导致微量条件反应的缺陷。结论:这些数据表明,在青春期间歇性暴露于乙醇会导致海马依赖性微量条件反射的损害,这种损害持续超过乙醇暴露期。延迟条件反射不受先前乙醇处理的影响,这表明在检测CS或US或参与冻结行为的能力方面没有困难。这些结果表明,青少年的大脑可能特别容易受到反复暴露于乙醇的影响,这会对非空间、海马依赖的认知能力产生影响。
Background:Recent studies have revealed that the adolescent brain may be especially vulnerable to ethanol‐induced toxicity. Corticolimbic regions are more severely damaged following ethanol exposure during adolescence than during adulthood. The consequences of adolescent ethanol exposure on cognition however, have only recently begun to be explored.Methods:Male and female rats were administered 0, 1.5, 2.5 or 4.5 g/kg ethanol (20% v/v) by acute intragastric gavage during adolescence (postnatal days [PD] 28, 30, 32 and 34). On PD 40, half of the subjects in each dose group were given 5 pairings of a 10‐sec flashing light (CS; conditioned stimulus) immediately followed by mild footshock (US; unconditioned stimulus), a procedure known as delay conditioning. The other half were also given 5 CS‐US pairings, but the US was presented 10 sec after CS offset, a procedure known as trace conditioning. All subjects were tested for CS‐elicited freezing 24 h later.Results:There was no effect of adolescent ethanol exposure on delay conditioned responding, with all subjects demonstrating comparable levels of CS‐elicited freezing. In contrast, the amount of freezing in the trace conditioned subjects was negatively correlated with prior ethanol dose. Specifically, exposure to 2.5 or 4.5 g/kg during adolescence resulted in a deficit in trace conditioned responding.Conclusions:These data indicate that intermittent exposure to ethanol during adolescence results in impairment in hippocampal‐dependent trace conditioning that persists beyond the period of ethanol exposure. Delay conditioning was unaffected by prior ethanol treatment, indicating that there was no difficulty in detecting the CS or US, or in the ability to engage in freezing behavior. These results suggest that the adolescent brain may be particularly vulnerable to the effects of repeated exposure to ethanol that can have consequences for nonspatial, hippocampal‐dependent cognitive abilities.
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发表时间: 1988
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影响因子: --
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期刊: Tissue Antigens
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影响因子: 6.2
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DOI: --
发表时间: 1987
影响因子: 4.4
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