Pittsburgh Hearing Research Center, Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PA, 15261, USA.
Departments of Neurobiology and Statistics, University of Chicago, Chicago, IL, 60637, USA.
Nat Commun. 2023 Jul 13;14(1):4170. doi: 10.1038/s41467-023-39732-7.
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.
外周感觉器官损伤导致代偿性皮质可塑性，这与皮质对声音反应的显著恢复有关。确切的机制解释了这种可塑性是如何实现的，以及如何在多样化的兴奋性和抑制性皮质神经元中分布，目前仍不清楚。在噪声损伤和持续的外周缺陷后，我们发现小鼠 A1 兴奋性主神经元（PNs）、表达 parvalbumin 和血管活性肠肽的神经元（PVs 和 VIPs）中恢复了声音诱发的活动，但表达 somatostatin 的神经元（SOMs）的活动减少。这种细胞类型特异性的恢复也与细胞类型特异性的内在可塑性有关。这些发现，以及我们的计算模型结果，与以下观点一致：PV 可塑性有助于 PN 的稳定性，SOM 可塑性允许增加 PN 和 PV 的活动，而 VIP 可塑性通过抑制 SOMs 来实现 PN 和 PV 的恢复。
