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突触前 GABA(B) 受体调节抑制性短期可塑性的经验依赖性发展。

Presynaptic GABA(B) receptors regulate experience-dependent development of inhibitory short-term plasticity.

机构信息

Center for Neural Science, New York University, New York, New York 10003, USA.

出版信息

J Neurosci. 2010 Feb 17;30(7):2716-27. doi: 10.1523/JNEUROSCI.3903-09.2010.

Abstract

Short-term changes in synaptic gain support information processing throughout the CNS, yet we know little about the developmental regulation of such plasticity. Here we report that auditory experience is necessary for the normal maturation of synaptic inhibitory short-term plasticity (iSTP) in the auditory cortex, and that presynaptic GABA(B) receptors regulate this development. Moderate or severe hearing loss was induced in gerbils, and iSTP was characterized by measuring inhibitory synaptic current amplitudes in response to repetitive stimuli. We reveal a profound developmental shift of iSTP from depressing to facilitating after the onset of hearing. Even moderate hearing loss prevented this shift. This iSTP change was mediated by a specific class of inhibitory interneurons, the low-threshold spiking cells. Further, using paired recordings, we reveal that presynaptic GABA(B) receptors at interneuron-pyramidal connections regulate iSTP in an experience-dependent manner. This novel synaptic mechanism may support the emergence of mature temporal processing in the auditory cortex.

摘要

短期突触增益变化支持中枢神经系统中的信息处理,但我们对这种可塑性的发育调节知之甚少。在这里,我们报告听觉经验对于听觉皮层中抑制性短期突触可塑性(iSTP)的正常成熟是必要的,并且突触前 GABA(B) 受体调节这种发育。在沙鼠中诱导中度或重度听力损失,并通过测量对重复刺激的抑制性突触电流幅度来表征 iSTP。我们揭示了听觉发生后 iSTP 从压抑到促进的深刻发育转变。即使是中度听力损失也阻止了这种转变。这种 iSTP 变化是由一类特定的抑制性中间神经元,即低阈值放电细胞介导的。此外,使用成对记录,我们揭示了中间神经元-锥体神经元连接上的突触前 GABA(B) 受体以经验依赖的方式调节 iSTP。这种新的突触机制可能支持听觉皮层中成熟的时间处理的出现。

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