Long-term synaptic plasticity is impaired in rats with lesions of the ventrolateral preoptic nucleus.
Long-term synaptic plasticity is impaired in rats with lesions of the ventrolateral preoptic nucleus.
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DOI：
10.1111/j.1460-9568.2009.07001.x
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发表时间：
2009-12-03
期刊：
影响因子：
--
通讯作者：
Saper CB
中科院分区：
文献类型：
--
作者：
Arrigoni E;Lu J;Vetrivelan R;Saper CB
在睡眠剥夺模型中经常报告记忆功能受损。类似地，海马长期突触可塑性已被证明对由于急性睡眠限制导致的睡眠丧失敏感。然而，这种方法受到睡眠剥夺的压力性质的限制，并且因为很难在动物中研究长期的睡眠限制。在这里，我们报告的影响，慢性睡眠剥夺对海马长时程增强（LTP）在啮齿动物模型慢性部分睡眠剥夺。我们研究了LTP的Schaffer侧支-CA 1突触在海马脑片制备的大鼠与病变的腹外侧视前核（VLPO），谁遭受减少总睡眠时间数周后病变。在从VLPO损伤大鼠制备的切片中，LTP受损与睡眠损失量成比例，LTP的下降遵循累积睡眠债务量的单一指数函数。与假损伤对照组相比，VLPO损伤大鼠的海马切片对腺苷拮抗剂和配对脉冲易化（PPF）的反应更大。然而，外源性腺苷在VLPO损伤和假损伤大鼠中抑制了诱发的突触传递并增加了等量的PPF，这表明VLPO损伤大鼠中更大的内源性腺苷抑制性音调与更大的配体积累相关，而不是腺苷受体敏感性或腺苷介导的神经递质释放概率的变化。在VLPO损伤的动物的LTP部分恢复腺苷拮抗剂表明，在VLPO损伤的动物腺苷积累可以解释一些观察到的突触可塑性缺陷。
Impairment of memory functions has been frequently reported in models of sleep deprivation. Similarly, hippocampal long-term synaptic plasticity has been shown to be sensitive to sleep loss due to acute sleep restriction. However, such approaches are limited by the stressful nature of sleep deprivation, and because it is difficult to study long term sleep restriction in animals. Here we report the effects of chronic sleep loss on hippocampal long-term potentiation (LTP) in a rodent model for chronic partial sleep deprivation. We studied LTP of the Schaffer collateral-CA1 synapses in hippocampal slices prepared from rats with lesions of the ventrolateral preoptic nucleus (VLPO), who suffer reduction in total sleep time for several weeks after lesions. In slices prepared from VLPO-lesioned rats, LTP was impaired proportional to the amount of sleep loss and the decline in LTP followed a single exponential function over the amount of accumulated sleep debt. As compared to sham-lesioned controls, hippocampal slices from VLPO-lesioned rats showed a greater response to adenosine antagonists and greater paired-pulse facilitation (PPF). However, exogenous adenosine depressed evoked synaptic transmission and increased PPF in VLPO-lesioned and sham-lesioned rats by equal amounts, suggesting that the greater endogenous adenosine inhibitory tone in the VLPO-lesioned rats is associated with greater ligand accumulation rather than a change in adenosine receptor sensitivity or adenosine-mediated neurotransmitter release probability. LTP in VLPO-lesioned animals was partially restored by adenosine antagonists suggesting that adenosine accumulation in VLPO-lesioned animals can account for some of the observed synaptic plasticity deficits.
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影响因子：
3.4
作者：
Arrigoni, Elda;Rosenberg, Paul A.
通讯作者：
Rosenberg, Paul A.
影响因子：
4.2
作者：
Alanko, L;Heiskanen, S;Porkka-Heiskanen, T
通讯作者：
Porkka-Heiskanen, T
影响因子：
2.9
作者：
ARAI, A;LYNCH, G
通讯作者：
LYNCH, G
影响因子：
2.9
作者：
Guan, ZW;Peng, XW;Fang, JD
通讯作者：
Fang, JD
影响因子：
3.3
作者：
DEMENDONCA, A;RIBEIRO, JA
通讯作者：
RIBEIRO, JA