Harvey Jenni, Solovyova Natasha, Irving Andrew
Neurosciences Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, Scotland, United Kingdom.
Prog Lipid Res. 2006 Sep;45(5):369-78. doi: 10.1016/j.plipres.2006.03.001. Epub 2006 Apr 21.
It is well documented that the hormone leptin plays a pivotal role in regulating food intake and body weight via its hypothalamic actions. However, leptin receptors are expressed throughout the brain with high levels found in the hippocampus. Evidence is accumulating that leptin has widespread actions on CNS function and in particular learning and memory. Recent studies have demonstrated that leptin-deficient or-insensitive rodents have impairments in hippocampal synaptic plasticity and in spatial memory tasks performed in the Morris water maze. Moreover, direct administration of leptin into the brain facilitates hippocampal long-term potentiation (LTP), and improves memory performance in mice. There is also evidence that, at the cellular level, leptin has the capacity to convert hippocampal short-term potentiation (STP) into LTP, via enhancing NMDA receptor function. Recent data indicates that leptin can also induce a novel form of NMDA receptor-dependent hippocampal long-term depression. Here, we review the evidence implicating a key role for the hormone leptin in modulating hippocampal synaptic plasticity and discuss the role of lipid signaling cascades in this process.
有充分的文献记载，激素瘦素通过其在下丘脑的作用，在调节食物摄入和体重方面发挥着关键作用。然而，瘦素受体在整个大脑中均有表达，在海马体中含量很高。越来越多的证据表明，瘦素对中枢神经系统功能，特别是学习和记忆具有广泛的作用。最近的研究表明，缺乏瘦素或对瘦素不敏感的啮齿动物在海马体突触可塑性以及在莫里斯水迷宫中进行的空间记忆任务方面存在缺陷。此外，将瘦素直接注入大脑可促进海马体长期增强作用（LTP），并改善小鼠的记忆表现。也有证据表明，在细胞水平上，瘦素能够通过增强NMDA受体功能，将海马体短期增强作用（STP）转化为LTP。最近的数据表明，瘦素还可以诱导一种新形式的NMDA受体依赖性海马体长期抑制。在此，我们综述了表明激素瘦素在调节海马体突触可塑性中起关键作用的证据，并讨论了脂质信号级联反应在此过程中的作用。
