scholarly journals Unmodified CdSe Quantum Dots Induce Elevation of Cytoplasmic Calcium Levels and Impairment of Functional Properties of Sodium Channels in Rat Primary Cultured Hippocampal Neurons

2008 ◽  
Vol 116 (7) ◽  
pp. 915-922 ◽  
Author(s):  
Mingliang Tang ◽  
Tairan Xing ◽  
Jie Zeng ◽  
Huili Wang ◽  
Chenchen Li ◽  
...  
2015 ◽  
Vol 112 (32) ◽  
pp. E4475-E4484 ◽  
Author(s):  
Yu-Hui Wong ◽  
Chia-Ming Lee ◽  
Wenjun Xie ◽  
Bianxiao Cui ◽  
Mu-ming Poo

Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation.


2021 ◽  
Vol 154 (1) ◽  
pp. 014301
Author(s):  
Elisabetta Collini ◽  
Hugo Gattuso ◽  
R. D. Levine ◽  
F. Remacle

2010 ◽  
Vol 245 ◽  
pp. 012067 ◽  
Author(s):  
I Concina ◽  
M M Natile ◽  
A Braga ◽  
A Vomiero ◽  
V Morandi ◽  
...  

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