Prenatal ethanol exposure persistently impairs NMDA receptor-dependent activation of extracellular signal-regulated kinase in the mouse dentate gyrus.
Prenatal ethanol exposure persistently impairs NMDA receptor-dependent activation of extracellular signal-regulated kinase in the mouse dentate gyrus.
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DOI：
10.1111/j.1471-4159.2009.06049.x
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发表时间：
2009-06
影响因子：
4.7
通讯作者：
Caldwell KK
中科院分区：
文献类型：
--
作者：
Samudio-Ruiz SL;Allan AM;Valenzuela CF;Perrone-Bizzozero NI;Caldwell KK
齿状回(DG)是海马区的中枢输入区，在学习和记忆中起着重要作用。先前的研究表明，出生前酒精与成年动物海马区依赖的学习缺陷和在DG中诱导长时程增强(LTP)的能力降低有关。鉴于N-甲基-D-天冬氨酸(NMDA)受体激活细胞外信号调节激酶1/2(ERK1/2)信号通路是各种形式的学习和记忆所必需的，以及包括DG在内的海马区的LTP，我们假设胎儿酒精暴露(FAE)成年动物在海马区NMDA受体依赖的ERK1/2激活方面存在缺陷。我们使用免疫印迹和免疫组织化学技术检测了NMDA刺激的成年FAE小鼠急性海马片ERK1/2的激活。我们首次提出了将产前酒精暴露与NMDA受体依赖的ERK1/2激活缺陷联系起来的证据，特别是在成年后代的DG中。这一缺陷可能解释了之前在DG中观察到的LTP缺陷，以及与产前酒精暴露相关的终生认知缺陷。
The dentate gyrus (DG) is the central input region to the hippocampus and is known to play an important role in learning and memory. Previous studies have shown that prenatal alcohol is associated with hippocampal-dependent learning deficits and a decreased ability to elicit long term potentiation (LTP) in the DG in adult animals. Given that activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling cascade by N-methyl-D-aspartate (NMDA) receptors is required for various forms of learning and memory, as well as LTP, in hippocampal regions, including the DG, we hypothesized that fetal alcohol-exposed (FAE) adult animals would have deficits in hippocampal NMDA receptor-dependent ERK1/2 activation. We used immunoblotting and immunohistochemistry techniques to detect NMDA-stimulated ERK1/2 activation in acute hippocampal slices prepared from adult FAE mice. We present the first evidence linking prenatal alcohol exposure to deficits in NMDA receptor-dependent ERK1/2 activation specifically in the DG of adult offspring. This deficit may account for the LTP deficits previously observed in the DG, as well as the life-long cognitive deficits, associated with prenatal alcohol exposure.
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影响因子：
4.8
作者：
Costa, ET;Olivera, DS;Valenzuela, CF
通讯作者：
Valenzuela, CF
影响因子：
2.9
作者：
BLANCHARD, BA;RILEY, EP;HANNIGAN, JH
通讯作者：
HANNIGAN, JH
影响因子：
2.7
作者：
GOODLETT, CR;PETERSON, SD
通讯作者：
PETERSON, SD
影响因子：
5.3
作者：
Kanterewicz, BI;Urban, NN;Klann, E
通讯作者：
Klann, E
影响因子：
2.7
作者：
Dillon, Gregory M.;Qu, Xianlu;Dodart, Jean-Cosme
通讯作者：
Dodart, Jean-Cosme