Ropp Tessa-Jonne F, Tiedemann Kerrie L, Young Eric D, May Bradford J
Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
J Assoc Res Otolaryngol. 2014 Dec;15(6):1007-22. doi: 10.1007/s10162-014-0488-2. Epub 2014 Sep 26.
This study describes the long-term effects of sound-induced cochlear trauma on spontaneous discharge rates in the central nucleus of the inferior colliculus (ICC). As in previous studies, single-unit recordings in Sprague-Dawley rats revealed pervasive increases in spontaneous discharge rates. Based on differences in their sources of input, it was hypothesized that physiologically defined neural populations of the auditory midbrain would reveal the brainstem sources that dictate ICC hyperactivity. Abnormal spontaneous activity was restricted to target neurons of the ventral cochlear nucleus. Nearly identical patterns of hyperactivity were observed in the contralateral and ipsilateral ICC. The elevation in spontaneous activity extended to frequencies well below and above the region of maximum threshold shift. This lack of frequency organization suggests that ICC hyperactivity may be influenced by regions of the brainstem that are not tonotopically organized. Sound-induced hyperactivity is often observed in animals with behavioral signs of tinnitus. Prior to electrophysiological recording, rats were screened for tinnitus by measuring gap pre-pulse inhibition of the acoustic startle reflex (GPIASR). Rats with positive phenotypes did not exhibit unique patterns of ICC hyperactivity. This ambiguity raises concerns regarding animal behavioral models of tinnitus. If our screening procedures were valid, ICC hyperactivity is observed in animals without behavioral indications of the disorder. Alternatively, if the perception of tinnitus is strictly linked to ongoing ICC hyperactivity, our current behavioral approach failed to provide a reliable assessment of tinnitus state.
本研究描述了声音诱发的耳蜗损伤对下丘中央核（ICC）自发放电率的长期影响。与之前的研究一样，在Sprague-Dawley大鼠中进行的单单位记录显示自发放电率普遍增加。基于其输入来源的差异，研究假设听觉中脑在生理上定义的神经群体将揭示决定ICC活动亢进的脑干来源。异常的自发放电活动仅限于蜗腹侧核的靶神经元。在对侧和同侧ICC中观察到几乎相同的活动亢进模式。自发放电活动的升高扩展到最大阈值偏移区域以下和以上的频率范围。这种缺乏频率组织的情况表明，ICC活动亢进可能受到脑干中并非按音频拓扑组织的区域的影响。在有耳鸣行为迹象的动物中经常观察到声音诱发的活动亢进。在进行电生理记录之前，通过测量听觉惊吓反射的间隙前脉冲抑制（GPIASR）对大鼠进行耳鸣筛查。具有阳性表型的大鼠并未表现出ICC活动亢进的独特模式。这种模糊性引发了对耳鸣动物行为模型的担忧。如果我们的筛查程序是有效的，那么在没有该疾病行为迹象的动物中也观察到了ICC活动亢进。或者，如果耳鸣的感知与正在进行的ICC活动亢进严格相关，那么我们目前的行为方法未能提供对耳鸣状态的可靠评估。
