Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Neuron. 2010 Mar 11;65(5):718-31. doi: 10.1016/j.neuron.2010.02.019.
Degraded sensory experience during critical periods of development can have adverse effects on brain function. In the auditory system, conductive hearing loss associated with childhood ear infections can produce long-lasting deficits in auditory perceptual acuity, much like amblyopia in the visual system. Here we explore the neural mechanisms that may underlie "amblyaudio" by inducing reversible monaural deprivation (MD) in infant, juvenile, and adult rats. MD distorted tonotopic maps, weakened the deprived ear's representation, strengthened the open ear's representation, and disrupted binaural integration of interaural level differences (ILD). Bidirectional plasticity effects were strictly governed by critical periods, were more strongly expressed in primary auditory cortex than inferior colliculus, and directly impacted neural coding accuracy. These findings highlight a remarkable degree of competitive plasticity between aural representations and suggest that the enduring perceptual sequelae of childhood hearing loss might be traced to maladaptive plasticity during critical periods of auditory cortex development.
在发育的关键时期，感觉体验受损会对大脑功能产生不良影响。在听觉系统中，与儿童期耳部感染相关的传导性听力损失会导致听觉感知锐度的长期缺陷，就像视觉系统中的弱视一样。在这里，我们通过在婴儿、幼鼠和成年大鼠中诱导可逆的单耳剥夺（MD）来探索可能构成“弱视听觉”的神经机制。MD 扭曲了音调地形图，削弱了剥夺耳的表示，增强了开放耳的表示，并破坏了两耳水平差异（ILD）的双耳整合。双向可塑性效应严格受关键期的制约，在初级听觉皮层中的表达比下丘更强，并且直接影响神经编码的准确性。这些发现突出了听觉表现之间存在显著的竞争可塑性，表明儿童听力损失的持久知觉后遗症可能可追溯到听觉皮层发育关键期的适应性可塑性。
