Cell-type-specific plasticity of inhibitory interneurons in the rehabilitation of auditory cortex after peripheral damage.
Cell-type-specific plasticity of inhibitory interneurons in the rehabilitation of auditory cortex after peripheral damage.
复制标题
外周损伤后听皮质康复中抑制性中间神经元的细胞类型特异性可塑性。
DOI：
10.1038/s41467-023-39732-7
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发表时间：
2023-07-13
影响因子：
16.6
通讯作者：
Tzounopoulos T
中科院分区：
文献类型：
--
作者：
Kumar M;Handy G;Kouvaros S;Zhao Y;Brinson LL;Wei E;Bizup B;Doiron B;Tzounopoulos T
外周感觉器官损伤导致补偿性皮层可塑性，这与皮层对声音的反应的显著恢复有关。解释这种可塑性如何在兴奋性和抑制性皮层神经元的不同集合中实现和分布的精确机制仍然未知。噪声创伤和持续的外周赤字后，我们发现恢复的声音诱发的活动在小鼠A1兴奋性主神经元（PN），小白蛋白和血管活性肠肽表达神经元（PV和VIP），但生长抑素表达神经元（SOM）的活动减少。这种细胞类型特异性恢复也与细胞类型特异性内在可塑性有关。这些发现与我们的计算建模结果沿着与PV可塑性有助于PN稳定性、SOM可塑性允许增加PN和PV活性以及VIP可塑性通过抑制SOM使PN和PV恢复的概念一致。外周感觉器官损伤导致代偿性皮层可塑性。在这里，作者表明，噪声创伤后，听觉皮层神经元显示细胞类型特异性可塑性的声音诱发和内在的属性。
Peripheral sensory organ damage leads to compensatory cortical plasticity that is associated with a remarkable recovery of cortical responses to sound. The precise mechanisms that explain how this plasticity is implemented and distributed over a diverse collection of excitatory and inhibitory cortical neurons remain unknown. After noise trauma and persistent peripheral deficits, we found recovered sound-evoked activity in mouse A1 excitatory principal neurons (PNs), parvalbumin- and vasoactive intestinal peptide-expressing neurons (PVs and VIPs), but reduced activity in somatostatin-expressing neurons (SOMs). This cell-type-specific recovery was also associated with cell-type-specific intrinsic plasticity. These findings, along with our computational modelling results, are consistent with the notion that PV plasticity contributes to PN stability, SOM plasticity allows for increased PN and PV activity, and VIP plasticity enables PN and PV recovery by inhibiting SOMs. Peripheral sensory organ damage leads to compensatory cortical plasticity. Here, the authors show that after noise trauma, auditory cortical neurons display cell-type-specific plasticity in their sound-evoked and intrinsic properties.
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