Department of Psychology, Institute of Neuroscience, University of Oregon, Eugene, OR, United States.
Front Neural Circuits. 2022 Sep 8;16:972157. doi: 10.3389/fncir.2022.972157. eCollection 2022.
A fundamental task faced by the auditory system is the detection of events that are signaled by fluctuations in sound. Spiking in auditory cortical neurons is critical for sound detection, but the causal roles of specific cell types and circuits are still mostly unknown. Here we tested the role of a genetically identified population of layer 4 auditory cortical neurons in sound detection. We measured sound detection using a common variant of pre-pulse inhibition of the acoustic startle response, in which a silent gap in background noise acts as a cue that attenuates startle. We used a Gpr26-Cre driver line, which we found expressed predominantly in layer 4 of auditory cortex. Photostimulation of these cells, which were responsive to gaps in noise, was sufficient to attenuate the startle reflex. Photosuppression of these cells reduced neural responses to gaps throughout cortex, and impaired behavioral gap detection. These data demonstrate that cortical Gpr26 neurons are both necessary and sufficient for top-down modulation of the acoustic startle reflex, and are thus likely to be involved in sound detection.
听觉系统面临的一个基本任务是检测由声音波动信号指示的事件。听觉皮质神经元的尖峰放电对于声音检测至关重要，但特定细胞类型和回路的因果作用在很大程度上仍然未知。在这里，我们测试了听觉皮质第 4 层中一种经基因鉴定的神经元群体在声音检测中的作用。我们使用声惊反射的前脉冲抑制的常见变体来测量声音检测，其中背景噪声中的静音间隙充当减弱惊跳的提示。我们使用了 Gpr26-Cre 驱动线，发现它主要在听觉皮层的第 4 层表达。对这些对噪声中的间隙有反应的细胞进行光刺激足以减弱惊跳反射。这些细胞的光抑制降低了整个皮层对间隙的神经反应，并损害了行为间隙检测。这些数据表明，皮质 Gpr26 神经元是自上而下调制声惊反射所必需的，并且可能参与声音检测。
