School of Human Sciences, University of Western Australia, Crawley, WA 6009, Australia.
School of Human Sciences, University of Western Australia, Crawley, WA 6009, Australia; School of Biological Sciences, University of Western Australia, Crawley, WA 6009, Australia; Perron Institute for Neurological and Translational Research, Crawley, WA 6009, Australia.
Hear Res. 2023 Nov;439:108891. doi: 10.1016/j.heares.2023.108891. Epub 2023 Sep 21.
Acoustic trauma (AT) induced hearing loss elicits plasticity throughout the central auditory pathway, including at the level of the medial geniculate nucleus (MGN). Hearing loss also results in altered neuronal responses in the amygdala, which is involved in sensory gating at the level of the MGN. However, whether these altered responses in the amygdala affect sensory gating at the level of the MGN requires further evaluation. The current study aimed to investigate the effects of AT-induced hearing loss on the functional connectivity between the amygdala and the MGN. Male Sprague-Dawley rats were exposed to either sham (n = 5; no sound) or AT (n = 6; 16 kHz, 1 h, 124 dB SPL) under full anaesthesia. Auditory brainstem response (ABR) recordings were made to determine hearing thresholds. Two weeks post-exposure, extracellular recordings were used to assess the effect of electrical stimulation of the amygdala on tone-evoked (sham n = 22; AT n = 30) and spontaneous (sham n = 21; AT n = 29) activity of single neurons in the MGN. AT caused a large temporary and small permanent ABR threshold shift. Electrical stimulation of the amygdala induced differential effects (excitatory, inhibitory, or no effect) on both tone-evoked and spontaneous activity. In tone-evoked activity, electrical stimulation at 300 µA, maximum current, caused a significantly larger reduction in firing rate in AT animals compared to sham, due to an increase in the magnitude of inhibitory effects. In spontaneous activity, there was also a significantly larger magnitude of inhibitory effects following AT. The findings confirm that activation of the amygdala results in changes in MGN neuronal activity, and suggest the functional connectivity between the amygdala and the MGN is significantly altered following AT and subsequent hearing loss.
声创伤（AT）引起的听力损失会引起中枢听觉通路的可塑性，包括内侧膝状体核（MGN）水平。听力损失还导致杏仁核神经元反应的改变，杏仁核参与 MGN 水平的感觉门控。然而，杏仁核中这些改变的反应是否会影响 MGN 水平的感觉门控，还需要进一步评估。本研究旨在探讨 AT 诱导的听力损失对杏仁核与 MGN 之间功能连接的影响。雄性 Sprague-Dawley 大鼠在全身麻醉下分别暴露于假处理（n=5；无声音）或 AT（n=6；16 kHz，1 h，124 dB SPL）。进行听觉脑干反应（ABR）记录以确定听力阈值。暴露后两周，进行细胞外记录以评估杏仁核电刺激对音调诱发（假处理 n=22；AT n=30）和自发（假处理 n=21；AT n=29）MGN 中单神经元活动的影响。AT 导致 ABR 阈值的大暂时和小永久性转变。杏仁核电刺激对音调诱发和自发活动均产生不同的影响（兴奋、抑制或无影响）。在音调诱发活动中，300 µA 的电刺激，最大电流，导致 AT 动物的放电率显著降低，这是由于抑制作用的幅度增加所致。在自发活动中，AT 后也存在抑制作用幅度显著增大的情况。这些发现证实了杏仁核的激活导致 MGN 神经元活动的变化，并表明 AT 及随后的听力损失后，杏仁核与 MGN 之间的功能连接发生了显著改变。
