Department of Otolaryngology/Head and Neck Surgery, Kresge Hearing Research Inst., The University of Michigan, 1100W Medical Center Drive, Ann Arbor, MI 48109, USA.
Brain Res. 2012 Nov 16;1485:95-107. doi: 10.1016/j.brainres.2012.08.037. Epub 2012 Aug 24.
Tinnitus is the perception of sound in the absence of a physical sound stimulus. It is thought to arise from aberrant neural activity within central auditory pathways that may be influenced by multiple brain centers, including the somatosensory system. Auditory-somatosensory (bimodal) integration occurs in the dorsal cochlear nucleus (DCN), where electrical activation of somatosensory regions alters pyramidal cell spike timing and rates of sound stimuli. Moreover, in conditions of tinnitus, bimodal integration in DCN is enhanced, producing greater spontaneous and sound-driven neural activity, which are neural correlates of tinnitus. In primary auditory cortex (A1), a similar auditory-somatosensory integration has been described in the normal system (Lakatos et al., 2007), where sub-threshold multisensory modulation may be a direct reflection of subcortical multisensory responses (Tyll et al., 2011). The present work utilized simultaneous recordings from both DCN and A1 to directly compare bimodal integration across these separate brain stations of the intact auditory pathway. Four-shank, 32-channel electrodes were placed in DCN and A1 to simultaneously record tone-evoked unit activity in the presence and absence of spinal trigeminal nucleus (Sp5) electrical activation. Bimodal stimulation led to long-lasting facilitation or suppression of single and multi-unit responses to subsequent sound in both DCN and A1. Immediate (bimodal response) and long-lasting (bimodal plasticity) effects of Sp5-tone stimulation were facilitation or suppression of tone-evoked firing rates in DCN and A1 at all Sp5-tone pairing intervals (10, 20, and 40 ms), and greater suppression at 20 ms pairing-intervals for single unit responses. Understanding the complex relationships between DCN and A1 bimodal processing in the normal animal provides the basis for studying its disruption in hearing loss and tinnitus models. This article is part of a Special Issue entitled: Tinnitus Neuroscience.
耳鸣是指在没有物理声音刺激的情况下感知到声音。据认为,它是由于中枢听觉通路中的异常神经活动引起的,这种异常活动可能受到包括躯体感觉系统在内的多个大脑中枢的影响。听觉-躯体感觉(双模态)整合发生在耳蜗背核(DCN)中,躯体感觉区域的电激活改变了锥体细胞的尖峰时间和声音刺激的速率。此外,在耳鸣的情况下,DCN 中的双模态整合增强,产生更大的自发性和声音驱动的神经活动,这些是耳鸣的神经相关物。在初级听觉皮层(A1)中,正常系统中也描述了类似的听觉-躯体感觉整合(Lakatos 等人,2007),其中亚阈值多感觉调制可能是皮质下多感觉反应的直接反映(Tyll 等人,2011)。本工作利用 DCN 和 A1 中的同时记录,直接比较了完整听觉通路中这些不同脑区的双模态整合。四叉形,32 通道电极放置在 DCN 和 A1 中,以在脊髓三叉神经核(Sp5)电激活存在和不存在的情况下同时记录音调诱发的单位活动。双模态刺激导致 DCN 和 A1 中单元和多单位对随后声音的反应产生持久的易化或抑制。Sp5-音调刺激的即时(双模态反应)和持久(双模态可塑性)效应是在所有 Sp5-音调配对间隔(10、20 和 40 ms)中 DCN 和 A1 中音调诱发放电率的易化或抑制,以及在 20 ms 配对间隔下对单个单位反应的更大抑制。了解正常动物中 DCN 和 A1 双模态处理之间的复杂关系为研究听力损失和耳鸣模型中其破坏提供了基础。本文是特刊“耳鸣神经科学”的一部分。