Cui, Lei

[["dc.bibliographiccitation.firstpage","E3131"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","E3140"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Stodieck, Sophia Katharina"],["dc.contributor.author","Goetze, Bianka"],["dc.contributor.author","Cui, Lei"],["dc.contributor.author","Wong, Man Ho"],["dc.contributor.author","Wenzel, Colin"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Loewel, Siegrid"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T09:55:51Z"],["dc.date.available","2018-11-07T09:55:51Z"],["dc.date.issued","2015"],["dc.description.abstract","During critical periods, all cortical neural circuits are refined to optimize their functional properties. The prevailing notion is that the balance between excitation and inhibition determines the onset and closure of critical periods. In contrast, we show that maturation of silent glutamatergic synapses onto principal neurons was sufficient to govern the duration of the critical period for ocular dominance plasticity in the visual cortex of mice. Specifically, postsynaptic density protein-95 (PSD-95) was absolutely required for experience-dependent maturation of silent synapses, and its absence before the onset of critical periods resulted in lifelong juvenile ocular dominance plasticity. Loss of PSD-95 in the visual cortex after the closure of the critical period reinstated silent synapses, resulting in reopening of juvenile-like ocular dominance plasticity. Additionally, silent synapse-based ocular dominance plasticity was largely independent of the inhibitory tone, whose developmental maturation was independent of PSD-95. Moreover, glutamatergic synaptic transmission onto parvalbumin-positive interneurons was unaltered in PSD-95 KO mice. These findings reveal not only that PSD-95-dependent silent synapse maturation in visual cortical principal neurons terminates the critical period for ocular dominance plasticity but also indicate that, in general, once silent synapses are consolidated in any neural circuit, initial experience-dependent functional optimization and critical periods end."],["dc.identifier.doi","10.1073/pnas.1506488112"],["dc.identifier.isi","000356251800009"],["dc.identifier.pmid","26015564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36839"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Progressive maturation of silent synapses governs the duration of a critical period"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","394"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","408"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Liu, Yanling"],["dc.contributor.author","Cui, Lei"],["dc.contributor.author","Schwarz, Martin K."],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T10:28:21Z"],["dc.date.available","2018-11-07T10:28:21Z"],["dc.date.issued","2017"],["dc.description.abstract","Spike timing-dependent synaptic plasticity (STDP) serves as a key cellular correlate of associative learning, which is facilitated by elevated attentional and emotional states involving activation of adrenergic signaling. At cellular levels, adrenergic signaling increases dendrite excitability, but the underlying mechanisms remain elusive. Here we show that activation of beta 2-adrenoceptors promoted STD long-term synaptic potentiation at mouse hippocampal excitatory synapses by inactivating dendritic Kv1.1-containing potassium channels, which increased dendrite excitability and facilitated dendritic propagation of postsynaptic depolarization, potentially improving coincidental activation of pre- and postsynaptic terminals. We further demonstrate that adrenergic modulation of Kv1.1 was mediated by the signaling scaffold SAP97, which, through direct protein-protein interactions, escorts beta 2 signaling to remove Kv1.1 from the dendrite surface. These results reveal a mechanism through which the postsynaptic signaling scaffolds bridge the aroused brain state to promote induction of synaptic plasticity and potentially to enhance spike timing and memory encoding."],["dc.identifier.doi","10.1016/j.neuron.2016.12.039"],["dc.identifier.isi","000396428200017"],["dc.identifier.pmid","28103480"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43400"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","1097-4199"],["dc.relation.issn","0896-6273"],["dc.title","Adrenergic Gate Release for Spike Timing-Dependent Synaptic Potentiation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]