Dendritic spine dynamics are thought to be substrates for motor learning and memory, and altered spine dynamics often lead to impaired performance. Here, we describe an exception to this rule by studying mice lacking paired immunoglobulin receptor B (PirB^−/−). Pyramidal neuron dendrites in PirB^−/− mice have increased spine formation rates and density. Surprisingly, PirB^−/− mice learn a skilled reaching task faster than wild-type (WT) littermates. Furthermore, stabilization of learning-induced spines is elevated in PirB^−/− mice. Mechanistically, single-spine uncaging experiments suggest that PirB is required for NMDA receptor (NMDAR)-dependent spine shrinkage. The degree of survival of newly formed spines correlates with performance, suggesting that increased spine stability is advantageous for learning. Acute inhibition of PirB function in M1 of adult WT mice increases the survival of learning-induced spines and enhances motor learning. These results demonstrate that there are limits on motor learning that can be lifted by manipulating PirB, even in adulthood.

树突棘动力学被认为是运动学习和记忆的基础，而改变的脊柱动力学通常会导致性能受损。在这里，我们通过研究缺乏配对免疫球蛋白受体 B ( PirB ^-/- )的小鼠来描述该规则的一个例外。PirB ^-/-小鼠的锥体神经元树突增加了脊柱形成率和密度。令人惊讶的是，PirB ^-/-小鼠比野生型 (WT) 同窝小鼠更快地学习熟练的伸手任务。此外， PirB中学习诱导的脊柱的稳定性升高^-/-老鼠。从机械上讲，单脊柱解压实验表明，PirB 是 NMDA 受体 (NMDAR) 依赖性脊柱收缩所必需的。新形成的脊柱的存活程度与表现相关，这表明增加的脊柱稳定性有利于学习。成年 WT 小鼠 M1 中 PirB 功能的急性抑制增加了学习诱导的脊柱的存活率并增强了运动学习。这些结果表明，即使在成年期，也可以通过操纵 PirB 来解除对运动学习的限制。