Center for Neural Science, New York University, NY 10003, USA.
Hear Res. 2011 Sep;279(1-2):140-8. doi: 10.1016/j.heares.2011.03.015. Epub 2011 Apr 2.
Functional inhibitory synapses form in auditory cortex well before the onset of normal hearing. However, their properties change dramatically during normal development, and many of these maturational events are delayed by hearing loss. Here, we review recent findings on the developmental plasticity of inhibitory synapse strength, kinetics, and GABAA receptor localization in auditory cortex. Although hearing loss generally leads to a reduction of inhibitory strength, this depends on the type of presynaptic interneuron. Furthermore, plasticity of inhibitory synapses also depends on the postsynaptic target. Hearing loss leads reduced GABAA receptor localization to the membrane of excitatory, but not inhibitory neurons. A reduction in normal activity in development can also affect the use-dependent plasticity of inhibitory synapses. Even moderate hearing loss can disrupt inhibitory short- and long-term synaptic plasticity. Thus, the cortex did not compensate for the loss of inhibition in the brainstem, but rather exacerbated the response to hearing loss by further reducing inhibitory drive. Together, these results demonstrate that inhibitory synapses are exceptionally dynamic during development, and deafness-induced perturbation of inhibitory properties may have a profound impact on auditory processing.
功能性抑制性突触早在正常听力出现之前就在听觉皮层中形成。然而,它们的特性在正常发育过程中会发生巨大变化,许多这些成熟事件都会因听力损失而延迟。在这里,我们回顾了关于听觉皮层中抑制性突触强度、动力学和 GABAA 受体定位的发育可塑性的最新发现。尽管听力损失通常会导致抑制强度降低,但这取决于前突神经元的类型。此外,抑制性突触的可塑性还取决于突触后靶标。听力损失导致 GABAA 受体定位减少到兴奋性神经元而不是抑制性神经元的膜上。发育过程中正常活动的减少也会影响抑制性突触的依赖使用可塑性。即使是中度听力损失也会破坏抑制性短期和长期突触可塑性。因此,大脑皮层并没有弥补脑干中抑制的丧失,而是通过进一步降低抑制性驱动来加剧对听力损失的反应。总之,这些结果表明,抑制性突触在发育过程中具有异常的动态性,而耳聋引起的抑制特性的干扰可能对听觉处理产生深远影响。