Stimulus-specific adaptation (SSA) is the reduction in responses to frequent stimuli (standards) that does not generalize to rare stimuli (deviants). We investigated the contribution of inhibition in auditory cortex to SSA using two-photon targeted cell-attached recordings and optogenetic manipulations in male mice. We characterized the responses of parvalbumin (PV)-, somatostatin (SST)-, and vasoactive intestinal polypeptide (VIP)-expressing interneurons of layer 2/3, and of serotonin receptor 5HT3a-expressing interneurons of layer 1. All populations showed early-onset SSA. Unexpectedly, the PV, SST, and VIP populations exhibited a substantial late component of evoked activity, often stronger for standard than for deviant stimuli. Optogenetic suppression of PV neurons facilitated pyramidal neuron responses substantially more (approximately x10) for deviants than for standards. VIP suppression decreased responses of putative PV neurons, specifically for standard but not for deviant stimuli. Thus, the inhibitory network does not generate cortical SSA, but powerfully controls its expression by differentially affecting the responses to deviants and to standards.

SIGNIFICANCE STATEMENT Stimulus-specific adaptation (SSA) reflects the growing complexity of auditory processing along the ascending auditory system. In the presence of SSA, neuronal responses depend not only on the stimulus itself but also on the history of stimulation. Strong SSA in the fast, ascending auditory pathway first occurs in cortex. Here we studied the role of the cortical inhibitory network in shaping SSA, showing that while cortical inhibition does not generate SSA, it powerfully controls its expression. We deduce that the cortical network contributes in crucial ways to the properties of SSA.

刺激特异性适应 (SSA) 是对不能推广到罕见刺激（偏差）的频繁刺激（标准）的反应减少。我们使用双光子靶向细胞附着记录和雄性小鼠的光遗传学操作研究了听觉皮层抑制对 SSA 的贡献。我们表征了第 2/3 层表达小白蛋白 (PV)、生长抑素 (SST) 和血管活性肠多肽 (VIP) 的中间神经元以及第 1 层表达血清素受体 5HT3a 的中间神经元的反应。所有人群都表现出早期发病 SSA。出乎意料的是，PV、SST 和 VIP 群体表现出诱发活动的大量晚期成分，通常比标准刺激更强。PV 神经元的光遗传学抑制大大促进了锥体神经元的反应（大约x 10) 偏差大于标准。VIP 抑制降低了假定的 PV 神经元的反应，特别是对标准刺激但对异常刺激没有反应。因此，抑制网络不会产生皮质 SSA，而是通过不同地影响对异常和标准的反应来强有力地控制其表达。

意义陈述刺激特异性适应 (SSA) 反映了听觉处理沿上行听觉系统日益复杂的情况。在存在 SSA 的情况下，神经元反应不仅取决于刺激本身，还取决于刺激的历史。快速上行听觉通路中的强 SSA 首先出现在皮层。在这里，我们研究了皮质抑制网络在塑造 SSA 中的作用，表明虽然皮质抑制不会产生 SSA，但它有力地控制了它的表达。我们推断皮层网络以关键方式对 SSA 的特性做出贡献。