Fast-spiking Cell to Pyramidal Cell Connections Are the Most Sensitive to Propofol-induced Facilitation of GABAergic Currents in Rat Insular Cortex
Fast-spiking Cell to Pyramidal Cell Connections Are the Most Sensitive to Propofol-induced Facilitation of GABAergic Currents in Rat Insular Cortex
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DOI：
10.1097/aln.0000000000000183
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发表时间：
2014-07-01
期刊：
影响因子：
8.8
通讯作者：
Kobayashi, Masayuki
中科院分区：
文献类型：
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作者：
Koyanagi, Yuko;Oi, Yoshiyuki;Kobayashi, Masayuki
背景：异丙酚促进-氨基丁酸介导的抑制性突触传递。在大脑皮层，-氨基丁酸能中间神经元靶向兴奋性锥体细胞(PYR)和快峰细胞(FS)以及非FS中间神经元。因此，异丙酚诱导的抑制性传递易化导致兴奋性和抑制性传入PYR的平衡发生改变。方法：采用多个全细胞膜片钳记录大鼠胰岛皮质氨基丁酸能中间神经元和PYR，观察异丙酚是否根据突触前和突触后细胞亚型而不同地调节抑制性突触后电流(IPSCs)。结果：异丙酚(10M)持续延长所有类型抑制性连接的单位IPSCs(UIPSCs)的衰减动力学，而不改变第二和第一uIPSCs幅度或故障率。FSPyr连接对uIPSC电荷传递的促进作用(2.2±0.5pC，n=36)大于FSFS/非FS连接(0.9+/-0.2pC，n=37)，而非FSPyr连接(0.3+/-0.1pC，n=15)和非FSFS/非FS连接(0.2+/-0.1pC，n=36)对uIPSC电荷传递的促进作用小于FSPyr/FS/Non-FS连接。结论：主抑制性连接(FSPyr)对异丙酚诱导的uIPSCs易化最为敏感，其作用机制可能与突触后机制有关。这种FSPyr连接中uIPSC的优先增强可能导致投射神经元的神经活动受到抑制，进而减少皮层局部回路的兴奋性输出。
Background: Propofol facilitates -aminobutyric acid-mediated inhibitory synaptic transmission. In the cerebral cortex, -aminobutyric acidergic interneurons target both excitatory pyramidal cells (Pyr) and fast-spiking (FS) and non-FS interneurons. Therefore, the propofol-induced facilitation of inhibitory transmission results in a change in the balance of excitatory and inhibitory inputs to Pyr. However, it is still unknown how propofol modulates -aminobutyric acidergic synaptic transmission in each combination of Pyr and interneurons.Methods: The authors examined whether propofol differentially regulates inhibitory postsynaptic currents (IPSCs) depending on the presynaptic and postsynaptic cell subtypes using multiple whole cell patch clamp recording from -aminobutyric acidergic interneurons and Pyr in rat insular cortex.Results: Propofol (10 M) consistently prolonged decay kinetics of unitary IPSCs (uIPSCs) in all types of inhibitory connections without changing paired-pulse ratio of the second to first uIPSC amplitude or failure rate. The FSPyr connections exhibited greater enhancement of uIPSC charge transfer (2.2 0.5 pC, n = 36) compared with that of FSFS/non-FS connections (0.9 +/- 0.2 pC, n = 37), whereas the enhancement of charge transfer in non-FSPyr (0.3 +/- 0.1 pC, n = 15) and non-FSFS/non-FS connections (0.2 +/- 0.1 pC, n = 36) was smaller to those in FSPyr/FS/non-FS. Electrical synapses between FS pairs were not affected by propofol.Conclusions: The principal inhibitory connections (FSPyr) are the most sensitive to propofol-induced facilitation of uIPSCs, which is likely mediated by postsynaptic mechanisms. This preferential uIPSC enhancement in FSPyr connections may result in suppressed neural activities of projection neurons, which in turn reduces excitatory outputs from cortical local circuits.