Postsynaptic mechanisms govern the differential excitation of cortical neurons by thalamic inputs.
Postsynaptic mechanisms govern the differential excitation of cortical neurons by thalamic inputs.
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DOI：
10.1523/jneurosci.5971-08.2009
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发表时间：
2009-07-15
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影响因子：
--
通讯作者：
Scanziani M
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文献类型：
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作者：
Hull C;Isaacson JS;Scanziani M
丘脑皮层（TC）传入神经通过在兴奋性规则发放主细胞（RS细胞）和抑制性快速发放中间神经元（FS细胞）上形成突触，将感觉输入中继到皮层。这种分歧在皮层躯体感觉处理的最早阶段协调兴奋与抑制方面起着至关重要的作用。虽然相同的TC传入纤维接触FS和RS细胞，FS细胞从单个TC传入纤维接收更大更快的兴奋性输入。在这里，我们表明，这种更大的丘脑FS细胞的兴奋发生通过GluR2缺乏AMPA受体（AMPAR），结果从4倍大的量子振幅相比，丘脑输入到RS细胞。丘脑传入也激活两种细胞类型的突触处的NMDA受体（NMDAR），但RS细胞NMDAR电流较慢，并在生理膜电位下传递更多电流。由于这些突触特化，缺乏GluR2的AMPAR选择性地维持RS细胞的前馈抑制，而NMDAR有助于RS细胞的尖峰，从而导致皮质复发性兴奋。因此，丘脑传入活动分为两条路线，依赖于独特的补充突触后AMPAR和NMDAR协调的动态平衡的兴奋和抑制的感觉输入进入皮层。
Thalamocortical (TC) afferents relay sensory input to the cortex by making synapses onto both excitatory regular-spiking principal cells (RS cells) and inhibitory fast-spiking interneurons (FS cells). This divergence plays a crucial role in coordinating excitation with inhibition during the earliest steps of somatosensory processing in the cortex. Although the same TC afferents contact both FS and RS cells, FS cells receive larger and faster excitatory inputs from individual TC afferents. Here, we show that this larger thalamic excitation of FS cells occurs via GluR2-lacking AMPA receptors (AMPARs), and results from a 4-fold larger quantal amplitude as compared to the thalamic inputs onto RS cells. Thalamic afferents also activate NMDA receptors (NMDARs) at synapses onto both cells types, yet RS cell NMDAR currents are slower and pass more current at physiological membrane potentials. Due to these synaptic specializations, GluR2-lacking AMPARs selectively maintain feedforward inhibition of RS cells, while NMDARs contribute to the spiking of RS cells and hence to cortical recurrent excitation. Thus, thalamic afferent activity diverges into two routes that rely on unique complements of postsynaptic AMPARs and NMDARs to orchestrate the dynamic balance of excitation and inhibition as sensory input enters the cortex.