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评估海马苔藓纤维突触中GLUK5和GLUK6的作用。

Assessing the role of GLUK5 and GLUK6 at hippocampal mossy fiber synapses.

作者信息

Breustedt Jörg, Schmitz Dietmar

机构信息

Neurowissenschaftliches Forschungszentrum, Charité Universitätsmedizin Berlin, 10117 Berlin, Germany.

出版信息

J Neurosci. 2004 Nov 10;24(45):10093-8. doi: 10.1523/JNEUROSCI.3078-04.2004.

DOI:10.1523/JNEUROSCI.3078-04.2004
PMID:15537878
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6730189/
Abstract

It has been suggested recently that presynaptic kainate receptors (KARs) are involved in short-term and long-term synaptic plasticity at hippocampal mossy fiber synapses. Using genetic deletion and pharmacology, we here assess the role of GLU(K5) and GLU(K6) in synaptic plasticity at hippocampal mossy fiber synapses. We found that the kainate-induced facilitation was completely abolished in the GLU(K6)-/- mice, whereas it was unaffected in the GLU(K5)-/-. Consistent with this finding, synaptic facilitation was reduced in the GLU(K6)(-/-) and was normal in the GLU(K5)-/-. In agreement with these results and ruling out any compensatory effects in the genetic deletion models, application of the GLU(K5)-specific antagonist LY382884 [(3S,4aR,6S,8aR)-6-(4-carboxyphenyl)methyl-1,2,3,4,4a,5,6,7,8,8a-decahydroisoquinoline-3-carboxylic acid] did not affect short-term and long-term synaptic plasticity at the hippocampal mossy fiber synapses. We therefore conclude that the facilitatory effects of kainate on mossy fiber synaptic transmission are mediated by GLU(K6)-containing KARs.

摘要

最近有人提出，突触前海人藻酸受体（KARs）参与海马苔藓纤维突触的短期和长期突触可塑性。我们利用基因敲除和药理学方法，评估了GLU(K5)和GLU(K6)在海马苔藓纤维突触可塑性中的作用。我们发现，海人藻酸诱导的易化在GLU(K6)-/-小鼠中完全消失，而在GLU(K5)-/-小鼠中未受影响。与此发现一致，GLU(K6)(-/-)小鼠的突触易化降低，而GLU(K5)-/-小鼠的突触易化正常。与这些结果一致，并排除基因敲除模型中的任何补偿效应，应用GLU(K5)特异性拮抗剂LY382884[（3S,4aR,6S,8aR）-6-（4-羧基苯基）甲基-1,2,3,4,4a,5,6,7,8,8a-十氢异喹啉-3-羧酸]不影响海马苔藓纤维突触的短期和长期突触可塑性。因此，我们得出结论，海人藻酸对苔藓纤维突触传递的易化作用是由含GLU(K6)的KARs介导的。

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