Intracortical circuits amplify sound-evoked activity in primary auditory cortex following systemic injection of salicylate in the rat.
Intracortical circuits amplify sound-evoked activity in primary auditory cortex following systemic injection of salicylate in the rat.
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DOI：
10.1152/jn.00946.2011
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发表时间：
2012-07
影响因子：
2.5
通讯作者：
D. Stolzberg;Michael Chrostowski;R. Salvi;B. Allman
中科院分区：
文献类型：
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作者：
D. Stolzberg;Michael Chrostowski;R. Salvi;B. Allman
高剂量的水杨酸钠会暂时引起人类和其他动物的耳鸣、轻度听力损失，并可能导致听力过敏。水杨酸盐对耳蜗功能具有明确的影响，主要导致大脑听觉输入的适度减少。尽管外周敏感性和输出降低，水杨酸盐却在初级听觉皮层（A1）水平诱导声诱发场电位的反常增强。先前的电生理学研究已经开始描述 A1 丘脑受体层的变化；然而，A1 是一个复杂的神经回路，具有反复的皮质内连接。为了描述急性全身水杨酸盐治疗对 A1 层丘脑和皮质内声音驱动活动的影响，我们对麻醉大鼠皮质层采样的场电位应用电流源密度 (CSD) 分析。 CSD图的通常特征是颗粒层中存在大的、短潜伏期的、单突触的、丘脑驱动的下沉，随后是颗粒层上的振幅较低、潜伏期较长、多突触的、皮质内驱动的下沉。全身施用水杨酸盐后，在较高声级下颗粒和颗粒上的下沉幅度几乎加倍。超颗粒汇振幅输入/输出函数从大约 50 dB 渐近变为急剧非渐近，通常在较高声级下主导颗粒汇振幅。颗粒上池还表现出峰值潜伏期的显着减少，反映了声音诱发反应的皮质内处理的加速。此外，水杨酸盐改变了多单位（MU）活性；在颗粒层和颗粒下层中，正常发作/持续的 MU 反应类型转变为主要发作反应类型。 CSD 分析结果表明，水杨酸盐通过皮质内回路显着增强声音驱动的反应。
A high dose of sodium salicylate temporarily induces tinnitus, mild hearing loss, and possibly hyperacusis in humans and other animals. Salicylate has well-established effects on cochlear function, primarily resulting in the moderate reduction of auditory input to the brain. Despite decreased peripheral sensitivity and output, salicylate induces a paradoxical enhancement of the sound-evoked field potential at the level of the primary auditory cortex (A1). Previous electrophysiologic studies have begun to characterize changes in thalamorecipient layers of A1; however, A1 is a complex neural circuit with recurrent intracortical connections. To describe the effects of acute systemic salicylate treatment on both thalamic and intracortical sound-driven activity across layers of A1, we applied current-source density (CSD) analysis to field potentials sampled across cortical layers in the anesthetized rat. CSD maps were normally characterized by a large, short-latency, monosynaptic, thalamically driven sink in granular layers followed by a lower amplitude, longer latency, polysynaptic, intracortically driven sink in supragranular layers. Following systemic administration of salicylate, there was a near doubling of both granular and supragranular sink amplitudes at higher sound levels. The supragranular sink amplitude input/output function changed from becoming asymptotic at approximately 50 dB to sharply nonasymptotic, often dominating the granular sink amplitude at higher sound levels. The supragranular sink also exhibited a significant decrease in peak latency, reflecting an acceleration of intracortical processing of the sound-evoked response. Additionally, multiunit (MU) activity was altered by salicylate; the normally onset/sustained MU response type was transformed into a primarily onset response type in granular and infragranular layers. The results from CSD analysis indicate that salicylate significantly enhances sound-driven response via intracortical circuits.