内稳态可塑性驱动动物模型中的耳鸣感知。
Homeostatic plasticity drives tinnitus perception in an animal model.
机构信息
Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA.
出版信息
Proc Natl Acad Sci U S A. 2011 Sep 6;108(36):14974-9. doi: 10.1073/pnas.1107998108.
Hearing loss often results in tinnitus and auditory cortical map changes, leading to the prevailing view that the phantom perception is associated with cortical reorganization. However, we show here that tinnitus is mediated by a cortical area lacking map reorganization. High-frequency hearing loss results in two distinct cortical regions: a sensory-deprived region characterized by a decrease in inhibitory synaptic transmission and a normal hearing region showing increases in inhibitory and excitatory transmission and map reorganization. Hearing-lesioned animals displayed tinnitus with a pitch in the hearing loss range. Furthermore, drugs that enhance inhibition, but not those that reduce excitation, reversibly eliminated the tinnitus behavior. These results suggest that sensory deprivation-induced homeostatic down-regulation of inhibitory synapses may contribute to tinnitus perception. Enhancing sensory input through map reorganization may plausibly alleviate phantom sensation.
听力损失常导致耳鸣和听觉皮质图谱变化，这导致了一种流行观点，即幻听与皮质重组有关。然而，我们在这里表明，耳鸣是由一个缺乏图谱重组的皮质区域介导的。高频听力损失导致两个不同的皮质区域：一个感觉剥夺区域，其特征是抑制性突触传递减少，一个正常听力区域，表现为抑制性和兴奋性传递增加和图谱重组。听力受损的动物表现出与听力损失范围一致的耳鸣音调。此外，增强抑制但不减少兴奋的药物可逆转消除耳鸣行为。这些结果表明，感觉剥夺诱导的抑制性突触的代偿性下调可能有助于耳鸣感知。通过图谱重组增强感觉输入可能合理地减轻幻听。
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