PDF(Pubmed)
Abstract：
Parvalbumin-expressing inhibitory neurons (PVNs) stabilize cortical network activity, generate gamma rhythms, and regulate experience-dependent plasticity. Here, we observed that activation or inactivation of PVNs functioned like a volume knob in the mouse auditory cortex (ACtx), turning neural and behavioral classification of sound level up or down over a 20dB range. PVN loudness adjustments were \"sticky\", such that a single bout of 40Hz PVN stimulation sustainably suppressed ACtx sound responsiveness, potentiated feedforward inhibition, and behaviorally desensitized mice to loudness. Sensory sensitivity is a cardinal feature of autism, aging, and peripheral neuropathy, prompting us to ask whether PVN stimulation can persistently desensitize mice with ACtx hyperactivity, PVN hypofunction, and loudness hypersensitivity triggered by cochlear sensorineural damage. We found that a single 16-minute bout of 40Hz PVN stimulation session restored normal loudness perception for one week, showing that perceptual deficits triggered by irreversible peripheral injuries can be reversed through targeted cortical circuit interventions.
摘要：
表达小白蛋白的抑制性神经元（PVNs）稳定皮层网络活动，产生伽马节律,并调节经验依赖的可塑性。这里,我们观察到PVNs的激活或失活的功能就像鼠标听觉皮层（ACtx）的音量旋钮，在20dB范围内向上或向下调整声级的神经和行为分类。PVN响度调整为“粘性”，这样一次40HzPVN刺激可持续抑制ACTX声音响应，增强前馈抑制，和对响度的行为脱敏小鼠。感觉敏感是自闭症的主要特征，老化，和周围神经病变，提示我们询问PVN刺激是否可以使ACtx多动症的小鼠持续脱敏，PVN功能减退，和由耳蜗感觉神经性损伤引起的响度超敏反应。我们发现，一次16分钟的40HzPVN刺激会话恢复正常的响度感知一周，显示由不可逆的外周损伤引发的感知缺陷可以通过有针对性的皮质回路干预来逆转。
