Higher-Order Thalamocortical Inputs Gate Synaptic Long-Term Potentiation via Disinhibition
Higher-Order Thalamocortical Inputs Gate Synaptic Long-Term Potentiation via Disinhibition
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DOI：
10.1016/j.neuron.2018.10.049
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发表时间：
2019-01-02
期刊：
影响因子：
16.2
通讯作者：
Holtmaat, Anthony
中科院分区：
文献类型：
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作者：
Williams, Leena E.;Holtmaat, Anthony
感觉经验和知觉学习改变了皮层锥体神经元（PNs）的感受野特性，这在很大程度上是由突触长时程增强（LTP）介导的。皮层LTP的电路机制尚不清楚。在小鼠躯体感觉皮层，节律性地刺激触须可在2/3层PNs诱发LTP。我们在丘脑皮层切片中解剖了这种可塑性背后的突触回路。我们发现，从高阶，后内侧丘脑复合体（POm）的预测是关键，引发N-甲基-D-天冬氨酸受体（NMDAR）依赖的皮层内突触的LTP。配对激活皮质和高阶丘脑皮质输入增加血管活性肠肽（VIP）和小白蛋白（PV）中间神经元（IN）的活性和降低生长抑素（SST）IN活性，这一起解除抑制PN。VIP IN介导的去抑制是诱导LTP的关键。这项研究揭示了一个电路基序，其中高阶丘脑输入门突触可塑性通过去抑制。这个基序可以允许上下文反馈来塑造处理一阶感觉信息的突触回路。
Sensory experience and perceptual learning changes receptive field properties of cortical pyramidal neurons (PNs), largely mediated by synaptic long-term potentiation (LTP). The circuit mechanisms underlying cortical LTP remain unclear. In the mouse somatosensory cortex, LTP can be elicited in layer 2/3 PNs by rhythmic whisker stimulation. We dissected the synaptic circuitry underlying this type of plasticity in thalamocortical slices. We found that projections from higher-order, posterior medial thalamic complex (POm) are key to eliciting N-methyl-D-aspartate receptor (NMDAR)-dependent LTP of intracortical synapses. Paired activation of cortical and higher-order thalamocortical inputs increased vasoactive intestinal peptide (VIP) and parvalbumin (PV) interneuron (IN) activity and decreased somatostatin (SST) IN activity, which together disinhibited the PNs. VIP IN-mediated disinhibition was critical for inducing LTP. This study reveals a circuit motif in which higher-order thalamic inputs gate synaptic plasticity via disinhibition. This motif may allow contextual feedback to shape synaptic circuits that process first-order sensory information.