Timing and location of nicotinic activity enhances or depresses hippocampal synaptic plasticity
Timing and location of nicotinic activity enhances or depresses hippocampal synaptic plasticity
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DOI：
10.1016/s0896-6273(01)00332-4
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发表时间：
2001-07-19
期刊：
影响因子：
16.2
通讯作者：
Dani, JA
中科院分区：
文献类型：
--
作者：
Ji, D;Lape, R;Dani, JA
本研究揭示了尼古丁对小鼠注意力、记忆和认知影响的机制。突触可塑性的诱导，通过普遍接受的机制产生，是由烟碱乙酰胆碱受体调节的。锥体神经元中适当时间的尼古丁活性通过突触前和突触后通路促进了长期增强的诱导。另一方面，中间神经元上的尼古丁活性抑制附近锥体神经元，从而阻止或减少突触增强的诱导。突触调节依赖于烟碱活性的位置和时间。这些突触机制的丧失可能导致阿尔茨海默病期间的认知缺陷，这与胆碱能投射的丧失和尼古丁受体数量的减少有关。
This study reveals mechanisms in the mouse hippocampus that may underlie nicotinic influences on attention, memory, and cognition. Induction of synaptic plasticity, arising via generally accepted mechanisms, is modulated by nicotinic acetylcholine receptors. Properly timed nicotinic activity at pyramidal neurons boosted the induction of long-term potentiation via presynaptic and postsynaptic pathways. On the other hand, nicotinic activity on interneurons inhibited nearby pyramidal neurons and thereby prevented or diminished the induction of synaptic potentiation. The synaptic modulation was dependent on the location and timing of the nicotinic activity. Loss of these synaptic mechanisms may contribute to the cognitive deficits experienced during Alzheimer's diseases, which is associated with a loss of cholinergic projections and with a decrease in the number of nicotinic receptors.