The Auditory laboratory, School of Human Sciences, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia.
The Auditory laboratory, School of Human Sciences, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia.
Hear Res. 2021 Apr;403:108190. doi: 10.1016/j.heares.2021.108190. Epub 2021 Jan 30.
The mechanism of tinnitus, the perception of sound in the absence of acoustic stimulation, remains as yet unknown. It has been proposed that tinnitus is caused by altered spontaneous activity in the auditory pathway following cochlear damage in combination with inadequate gating at the level of the auditory thalamus, the medial geniculate nucleus (MGN). To investigate this further we made electrophysiological recordings in MGN of guinea pigs (n = 9) with and without tinnitus after acoustic trauma (continuous loud tone at 10 kHz, 124 dB SPL for 2 h). Parameters of interest were spontaneous tonic and burst firing. After acoustic trauma, 5 out of 9 guinea pigs developed signs of tinnitus as determined by the gap prepulse inhibition of acoustic startle. Spontaneous firing rates were significantly increased in the tinnitus animals as compared to the non-tinnitus animals and this change was specific to pure-tone responsive MGN neurons. However, burst firing parameters, including number of bursts per minute, burst duration, number of spikes in each burst, and percentage of spikes occurring in a burst, were not different between tinnitus and non-tinnitus animals. In addition, our data showed a strong dependence of spontaneous firing rates with heart rate, which implies that monitoring physiological status in animals is pertinent to obtaining reliable data when recording at higher levels of the auditory pathway. Our results suggest that increases in the tonic spontaneous fining rate of pure-tone responsive MGN neurons but not changes in burst firing parameters, are a robust neural signature of tinnitus in anaesthetised animals.
耳鸣的机制，即在没有声音刺激的情况下感知声音，目前仍然未知。有人提出，耳鸣是由于耳蜗损伤后听觉通路中自发性活动的改变，以及听觉丘脑、内侧膝状体（MGN）水平的门控不足引起的。为了进一步研究这一问题，我们在有和没有耳鸣的豚鼠（n=9）的 MGN 中进行了电生理记录，这些豚鼠在声学创伤后（连续 10 kHz 的强音，124 dB SPL 持续 2 小时）。感兴趣的参数是自发紧张和爆发性放电。在声学创伤后，9 只豚鼠中有 5 只出现了耳鸣的迹象，这是通过声学惊跳的间隙前脉冲抑制来确定的。与非耳鸣动物相比，耳鸣动物的自发放电率显著增加，这种变化是纯音反应性 MGN 神经元特有的。然而，爆发性放电参数，包括每分钟爆发次数、爆发持续时间、每个爆发中的尖峰数和爆发中尖峰的百分比，在耳鸣和非耳鸣动物之间没有差异。此外，我们的数据显示自发放电率与心率有很强的依赖性，这意味着在记录听觉通路较高水平时，监测动物的生理状态对于获得可靠的数据是很重要的。我们的结果表明，纯音反应性 MGN 神经元的紧张性自发放电率增加，但爆发性放电参数没有变化，这是麻醉动物耳鸣的一个强有力的神经特征。
