Synaptic Zinc Enhances Inhibition Mediated by Somatostatin, but not Parvalbumin, Cells in Mouse Auditory Cortex
Synaptic Zinc Enhances Inhibition Mediated by Somatostatin, but not Parvalbumin, Cells in Mouse Auditory Cortex
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DOI：
10.1093/cercor/bhaa005
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发表时间：
2020-07-01
期刊：
影响因子：
3.7
通讯作者：
Tzounopoulos, Thanos
中科院分区：
文献类型：
--
作者：
Kouvaros, Stylianos;Kumar, Manoj;Tzounopoulos, Thanos
皮层抑制对大脑活动和行为至关重要。然而，调节皮层抑制的机制及其对感觉处理的影响仍然不太清楚。突触释放的锌是一种由皮层神经元能突触囊泡释放的神经调质，已成为感觉加工和行为的强大调节剂。尽管令人困惑的发现，囊泡锌转运体（ZnT 3）mRNA表达在皮层抑制性中间神经元，突触锌在皮层抑制性神经传递的行动仍然未知。使用体外电生理学和光遗传学在小鼠大脑切片包含层2/3（L2/3）的听觉皮层，我们发现，突触锌增加抑制性GABA能神经传递的量子大小由生长抑素（SOM）介导的，但不是小清蛋白（PV）表达的神经元。使用双光子成像在清醒的小鼠，我们表明，突触锌是必需的SOM，但不是PV介导的抑制对频率调谐的主要神经元的影响。因此，皮层抑制的细胞特异性锌调节调节频率调谐。
Cortical inhibition is essential for brain activity and behavior. Yet, the mechanisms that modulate cortical inhibition and their impact on sensory processing remain less understood. Synaptically released zinc, a neuromodulator released by cortical glutamatergic synaptic vesicles, has emerged as a powerful modulator of sensory processing and behavior. Despite the puzzling finding that the vesicular zinc transporter (ZnT3) mRNA is expressed in cortical inhibitory interneurons, the actions of synaptic zinc in cortical inhibitory neurotransmission remain unknown. Using in vitro electrophysiology and optogenetics in mouse brain slices containing the layer 2/3 (L2/3) of auditory cortex, we discovered that synaptic zinc increases the quantal size of inhibitory GABAergic neurotransmission mediated by somatostatin (SOM)- but not parvalbumin (PV)-expressing neurons. Using two-photon imaging in awake mice, we showed that synaptic zinc is required for the effects of SOM- but not PV-mediated inhibition on frequency tuning of principal neurons. Thus, cell-specific zinc modulation of cortical inhibition regulates frequency tuning.