Pavlovian eyeblink conditioning has been used extensively to study the neural mechanisms underlying associative and motor learning. During this simple learning task, memory formation takes place at Purkinje cells in defined areas of the cerebellar cortex, which acquire a strong temporary suppression of their activity during conditioning. Yet, it is unknown which neuronal plasticity mechanisms mediate this suppression. Two potential mechanisms include long-term depression of parallel fiber to Purkinje cell synapses and feed-forward inhibition by molecular layer interneurons. We show, using a triple transgenic approach, that only concurrent disruption of both these suppression mechanisms can severely impair conditioning, highlighting that both processes can compensate for each other's deficits.

中文翻译：

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在没有抑制性输入的情况下，平行纤维对浦肯野细胞长期抑制的影响是无法掩盖的。

巴甫洛夫式眨眼条件已被广泛用于研究联想和运动学习的神经机制。在这个简单的学习任务中，小脑皮层限定区域内的Purkinje细胞发生记忆形成，这些细胞在调节过程中会暂时抑制其活动。然而，尚不清楚哪种神经元可塑性机制介导这种抑制。两种潜在的机制包括长期抑制平行纤维与浦肯野细胞突触的接触以及分子层中间神经元的前馈抑制作用。我们显示，使用三重转基因方法，只有同时抑制这两个抑制机制才能严重损害调节，这突出表明这两个过程可以弥补彼此的不足。