Fractalkine/CX3CL1 depresses central synaptic transmission in mouse hippocampal slices
Fractalkine/CX3CL1 depresses central synaptic transmission in mouse hippocampal slices
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DOI：
10.1016/j.neuropharm.2006.05.027
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发表时间：
2006-09-01
影响因子：
4.7
通讯作者：
Eusebi, Fabrizio
中科院分区：
文献类型：
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作者：
Bertollini, Cristina;Ragozzino, Davide;Eusebi, Fabrizio
这项工作报告了趋化因子 fractalkine/CX(3)CL1（一种在中枢神经系统中高度表达的内源性小肽）对使用电生理学方法在小鼠 CA1 辐射层中诱发的突触反应的影响。我们报道，在急性小鼠海马切片中，灌输 CX(3)CL1 导致场兴奋性突触后电位 (fEPSP) 可逆性降低，这种降低在几秒钟内出现，在应用后长达 10 分钟内增加，并在 CX(3)CL1 治疗结束后 30 分钟内消失。我们还表明，CX(3)CL1 诱导的突触抑制是 (i) 剂量依赖性，IC50 和 n(H) 值分别为 0.7 nM 和 1，(ii) 与配对脉冲促进的变化无关，(iii) 通过 CX(3)CL1 受体 (CX(3)CR1) 介导，在 CX(3)CR1(-/-) 小鼠中不存在，在 (iv) 通过诱导同突触长期抑制 (LTD) 来阻断野生型小鼠。我们得出结论，CX(3)CL1 是诱发兴奋性突触传递的有效神经调节剂，与 LTD 具有共同的机制。 (c) 2006 Elsevier Ltd. 保留所有权利。
This work reports the effect of chemokine fractalkine/CX(3)CL1, an endogenous small peptide highly expressed in the central nervous system, on evoked synaptic responses investigated in mouse CA1 stratum radiatum using an electrophysiological approach. We report that in acute mouse hippocampal slices, superfusion of CX(3)CL1 resulted in a reversible depression of the field excitatory postsynaptic potential (fEPSP) which developed within few seconds, increased for up to 10 min of application and disappeared within 30 min after the end of CX(3)CL1 treatment. We also show that CX(3)CL1-induced synaptic depression is (i) dose-dependent with IC50 and n(H) values of 0.7 nM and 1, respectively, (ii) not associated with a change in paired-pulse facilitation, (iii) mediated through CX(3)CL1 receptor (CX(3)CR1), being absent in CX(3)CR1(-/-) mice and inhibited in wild-type mice by a specific blocking antibody, and (iv) occluded by the induction of homosynaptic long-term depression (LTD). We conclude that CX(3)CL1 is a potent neuromodulator of the evoked excitatory synaptic transmission, sharing common mechanisms with LTD. (c) 2006 Elsevier Ltd. All rights reserved.