The nucleus accumbens is a critical integration center for reward-related circuitry and is comprised primarily of medium spiny projection neurons. The dynamic balance of excitation and inhibition onto medium spiny neurons determines the output of this structure. While nucleus accumbens excitatory synaptic plasticity is well-characterized, inhibitory synaptic plasticity mechanisms and their potential relevance to shaping motivated behaviors is poorly understood. Here we report the discovery of long-term depression of inhibitory synaptic transmission in the mouse nucleus accumbens core. This long-term depression is postsynaptically expressed, tropomyosin kinase B (TrkB) receptor-mediated, and augmented in the presence of ethanol. Our findings support the emerging view that TrkB signaling regulates inhibitory synaptic plasticity and suggest this mechanism in the nucleus accumbens as a target for ethanol modulation of reward.

中文翻译：

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TrkB依赖伏伏核的抑制作用被乙醇增强。

伏伏核是奖励相关电路的关键整合中心，主要由中突棘神经元组成。对中棘神经元的激发和抑制的动态平衡决定了这种结构的输出。虽然伏隔核的兴奋性突触可塑性具有良好的特征，但对抑制性突触可塑性的机制及其与塑造动机行为的潜在相关性了解甚少。在这里，我们报告鼠标伏伏核的抑制性突触传递的长期抑制的发现。这种长期的抑郁是突触后表达，原肌球蛋白激酶B（TrkB）受体介导的，并在乙醇存在下增强。