Contributions of receptor desensitization and saturation to plasticity at the retinogeniculate synapse
Contributions of receptor desensitization and saturation to plasticity at the retinogeniculate synapse
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DOI：
10.1016/s0896-6273(02)00611-6
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发表时间：
2002-02-28
期刊：
影响因子：
16.2
通讯作者：
Regehr, WG
中科院分区：
文献类型：
--
作者：
Chen, CF;Blitz, DM;Regehr, WG
视网膜膝状体突触将视觉信息从视网膜传递到丘脑中继神经元。在这里，我们研究了短期可塑性的机制，可以影响传输在这个连接在小鼠脑切片。我们的研究表明，由于在高频率下显著的抑制，突触强度被生理活动模式改变。突触后可塑性机制对这种突触抑制有重要作用。在视网膜输入刺激序列中，受体脱敏使AMPA EPSC衰减，而NMDA EPSC饱和。这种差异可塑性可能有助于解释这些受体在塑造中继神经元对视觉刺激的反应中的不同作用，AMPA组分对瞬态反应很重要，而持续的高频反应更多地依赖于NMDA组分。
The retinogeniculate synapse conveys visual information from the retina to thalamic relay neurons. Here, we examine the mechanisms of short-term plasticity that can influence transmission at this connection in mouse brain slices. Our studies show that synaptic strength is modified by physiological activity patterns due to marked depression at high frequencies. Postsynaptic mechanisms of plasticity make prominent contributions to this synaptic depression. During trains of retinal input stimulation, receptor desensitization attenuates the AMPA EPSC while the NMDA EPSC saturates. This differential plasticity may help explain the distinct roles of these receptors in shaping the relay neuron response to visual stimulation with the AMPA component being important for transient responses, while sustained high frequency responses rely more on the NMDA component.