Chronic nicotine exposure induces a long-lasting and pathway-specific facilitation of LTP in the amygdala.
Chronic nicotine exposure induces a long-lasting and pathway-specific facilitation of LTP in the amygdala.
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长期接触尼古丁会诱导杏仁核中 LTP 的持久且特定途径的促进。
DOI：
10.1101/lm.975308
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Levine,Amir
中科院分区：
文献类型：
--
作者：
Huang,Yan-You;Kandel,EricR;Levine,Amir
尼古丁，以烟草的形式，是最常用的滥用药物。除了有益的特性，尼古丁还影响许多认知和情绪过程，涉及几个大脑区域，包括海马体和杏仁核。药物暴露后，这些脑区突触强度的长期变化可能与尼古丁诱导的行为变化有重要关联。在这里，我们研究了长期口服尼古丁对杏仁核长期突触增强的影响，杏仁核是情绪记忆的关键结构。我们发现，口服尼古丁7d可显著增强杏仁核中的LTP。这种促进作用是通路特有的：尼古丁选择性地促进皮质-杏仁外侧核通路的LTP，而不是丘脑-外侧和外侧-基底外侧突触通路的LTP。尼古丁暴露7d所诱导的突触易化作用是持久的，停用尼古丁后持续72h，停用8d后衰退。相反，较短的尼古丁暴露(24小时)只会导致突触可塑性的短暂促进，这种促进作用在尼古丁停止24和72小时后消失。尼古丁暴露后杏仁核长时程增强的促进作用是通过消除GABA能抑制而实现的，依赖于激活的N-甲基-D-天冬氨酸受体，并且可以通过阻断α-7或β-2-NACH受体来阻止。我们的结果表明，长期接触尼古丁可以促进杏仁核特定通路中突触的长期改变，这些突触可塑性的变化可能有助于尼古丁引起的复杂的神经适应和行为。
Nicotine, in the form of tobacco, is the most commonly used drug of abuse. In addition to its rewarding properties, nicotine also affects many cognitive and emotional processes that involve several brain regions, including hippocampus and amygdala. Long-term changes in synaptic strength in these brain regions after drug exposure may be importantly correlated with behavioral changes induced by nicotine. Here, we study the effect of chronic oral administration of nicotine on the long-term synaptic potentiation in the amygdala, a key structure for emotional memory. We find that oral administration of nicotine for 7 d produces a significant enhancement of LTP in the amygdala. This facilitation is pathway specific: Nicotine selectively facilitates LTP in the cortical-lateral amygdala pathway, but not the thalamic-lateral and the lateral-basolateral synaptic pathway. The synaptic facilitation induced by a 7-d exposure to nicotine is long-lasting, it persists for 72 h after cessation of nicotine but decays 8 d after its cessation. In contrast, a shorter exposure of nicotine (24 h) induces only a short-lasting facilitation of synaptic plasticity that dissipates 24 and 72 h after cessation of nicotine. The facilitation of LTP in the amygdala after exposure to nicotine is mediated by removal of GABAergic inhibition, is dependent on the activation NMDA receptors, and can be prevented by blocking either α7 or β2 nACh receptors. Our results indicate that chronic exposure to nicotine can promote the induction of long-lasting modifications of synapses in a specific pathway in the amygdala.These changes in synaptic plasticity may contribute to the complex neural adaptations and behaviors caused by nicotine.
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