Abstract：
:Dendritic spines, a special kind of structure in nerve cells, play a key role in performing cellular function. Structural abnormalities of the dendritic spine may contribute to synaptic dysfunction and have been implicated in memory formation. However, the molecular mechanisms that trigger dendritic spine loss remain unclear. Here, we show that the absence of dendritic cell factor 1 (Dcf1) appeared dendritic spines dysplasia, which in turn leads to the damage of learning and memory; in contrast, enhancing Dcf1 expression rescues dendritic spines morphology and function, indicating a pivotal role of Dcf1 in cellular function. Electrophysiological test indicates that there is a significant reduction in the frequency of miniature excitatory postsynaptic currents in Dcf1 -/- knockout (KO) mice. Subsequent to optogenetic ignition, we observed a weaker neuronal activation in Dcf1 KO mice, explaining the neural circuit cause. On molecular mechanism, we demonstrated an unprecedented discovery that Dcf1 triggers the dendritic spine and synaptic function through the recruitment of Lcn2 and activation of PSD95-NMDAR signaling. Removing this brake leads to memory damage. Our results highlight an unexpected regulatory mechanism of dendritic spine development and formation.
journal_name
Mol Neurobioljournal_title
Molecular neurobiologyauthors
Liu Q,Feng R,Chen Y,Luo G,Yan H,Chen L,Lin R,Ding Y,Wen Tdoi
10.1007/s12035-016-0349-6subject
Has Abstractpub_date
2018-01-01 00:00:00pages
763-775issue
1eissn
0893-7648issn
1559-1182pii
10.1007/s12035-016-0349-6journal_volume
55pub_type
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