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The central amygdala recruits mesocorticolimbic circuitry for pursuit of reward or pain

机译:中央杏仁达拉促进培养奖励或痛苦的梅西科莫博

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How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions are created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. We find that pairings make the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruit mesocorticolimbic incentive-related circuitry. Shock-associated cues also gain positive incentive value and are pursued. Yet the motivational effects of paired CeA stimulation can be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increases defensive reactions. Finally, CeA ChR2 valence can be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.
机译:脑机制如何创造不良景点?在这里,通过对大鼠氨基葡聚糖(CEA)中央核的致盲肠梗阻(CHR2)刺激在遇到蔗糖,可卡因或痛苦的休克交付物体的大鼠中,在实验室大鼠中产生强烈的不良吸引力。我们发现配对使各种大鼠专门追求蔗糖,或专门的可卡因,或者反复自我造成冲击。 CEA诱导的适应性景点,甚至到痛苦的震荡棒,招募Mesocorticolimbic激励相关电路。冲击相关的提示也获得了积极的激励价值并进行了追求。然而,配对CEA刺激的励磁作用可以在Pavlovian恐惧学习情况下逆转到负效果,其中CEA CHR2配对增加防御性反应。最后,通过与无害的刺激配对,可以切换CEA CHR2价。这些结果揭示了在CEA激活的控制下通过Mesocorticolimbic电路的替补塑性和多种模式。

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