Department of Neurosciences, NE-63, Lerner Research Institute/Head and Neck Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44122, USA.
Hear Res. 2011 Jun;276(1-2):52-60. doi: 10.1016/j.heares.2010.12.003. Epub 2010 Dec 10.
Over the past decade, there has been a burgeoning of scientific interest in the neurobiological origins of tinnitus. During this period, numerous behavioral and physiological animal models have been developed which have yielded major clues concerning the likely neural correlates of acute and chronic forms of tinnitus and the processes leading to their induction. The data increasingly converge on the view that tinnitus is a systemic problem stemming from imbalances in the excitatory and inhibitory inputs to auditory neurons. Such changes occur at multiple levels of the auditory system and involve a combination of interacting phenomena that are triggered by loss of normal input from the inner ear. This loss sets in motion a number of plastic readjustments in the central auditory system and sometimes beyond the auditory system that culminate in the induction of aberrant states of activation that include hyperactivity, bursting discharges and increases in neural synchrony. This article will review was has been learned about the biological origins of these alterations, summarize where they occur and examine the cellular and molecular mechanisms that are most likely to underlie them.
在过去的十年中,人们对耳鸣的神经生物学起源产生了浓厚的兴趣。在此期间,已经开发出许多行为和生理动物模型,这些模型为急性和慢性耳鸣形式的可能神经相关性以及导致其产生的过程提供了主要线索。这些数据越来越倾向于认为,耳鸣是一种系统性问题,源于听觉神经元的兴奋和抑制输入失衡。这种变化发生在听觉系统的多个层次上,涉及一系列相互作用的现象,这些现象是由内耳正常输入的丧失引发的。这种丧失引发了中枢听觉系统的一系列可塑性调整,有时甚至超出了听觉系统,最终导致异常激活状态的诱导,包括过度活跃、爆发性放电和神经同步性增加。本文将回顾这些改变的生物学起源,总结它们发生的位置,并研究最有可能成为其基础的细胞和分子机制。