Bauer Carol A, Brozoski Thomas J
Southern Illinois University School of Medicine, Division of Otolaryngology Head and Neck Surgery, Springfield, IL 62794, USA.
Prog Brain Res. 2007;166:287-301. doi: 10.1016/S0079-6123(07)66027-0.
Several lines of evidence suggest that loss of central inhibition after deprivation of input from the ear (peripheral deafferentation) may be one cause of chronic tinnitus. Aging and acoustic trauma, the two most common causes of peripheral damage to the auditory system, each decrease input to central auditory structures. Loss of input to tonic inhibitory systems would release excitatory structures from inhibitory regulation. The increased activity resulting may be interpreted by more rostral structures in the auditory pathway as tinnitus. Down-regulation of gamma-amino butyric acid (GABA), a major inhibitory neurotransmitter of the central auditory pathway, is a potential mechanism for the loss of inhibition. Both animal studies and human clinical trials implicate loss of inhibition, and specifically loss of GABA function, in the development of acoustic trauma-induced tinnitus.
多条证据表明,耳部输入缺失(外周去传入)后中枢抑制的丧失可能是慢性耳鸣的一个原因。衰老和声学创伤是听觉系统外周损伤的两个最常见原因,它们各自都会减少对中枢听觉结构的输入。紧张性抑制系统输入的丧失会使兴奋性结构从抑制调节中释放出来。由此产生的活动增加可能会被听觉通路中更靠前的结构解读为耳鸣。γ-氨基丁酸(GABA)是中枢听觉通路的一种主要抑制性神经递质,其下调是抑制丧失的一种潜在机制。动物研究和人体临床试验均表明,抑制丧失,尤其是GABA功能丧失,与声学创伤性耳鸣的发生有关。