Cocaine inverts rules for synaptic plasticity of glutamate transmission in the ventral tegmental area
Cocaine inverts rules for synaptic plasticity of glutamate transmission in the ventral tegmental area
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DOI：
10.1038/nn.2763
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发表时间：
2011-04-01
影响因子：
25
通讯作者：
Luescher, Christian
中科院分区：
文献类型：
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作者：
Mameli, Manuel;Bellone, Camilla;Luescher, Christian
药物引起的突触可塑性影响奖赏回路的方式在很大程度上仍然难以捉摸。我们发现，可卡因减少了NMDA受体兴奋性突触后电流，并插入了缺乏GluA2的AMPA受体。因此，结合谷氨酸释放和超极化电流注射的刺激方案进一步加强了可卡因治疗后的突触。我们的数据表明，腹侧被盖区可卡因诱发的早期可塑性逆转了依赖活动的可塑性的规则，最终导致成瘾行为。
The manner in which drug-evoked synaptic plasticity affects reward circuits remains largely elusive. We found that cocaine reduced NMDA receptor excitatory postsynaptic currents and inserted GluA2-lacking AMPA receptors in dopamine neurons of mice. Consequently, a stimulation protocol pairing glutamate release with hyperpolarizing current injections further strengthened synapses after cocaine treatment. Our data suggest that early cocaine-evoked plasticity in the ventral tegmental area inverts the rules for activity-dependent plasticity, eventually leading to addictive behavior.