Sirtuin 3 is required for the protective effect of Resveratrol on Manganese‐induced disruption of mitochondrial biogenesis in primary cultured neurons

2020 ◽  
Author(s):  
Qian Sun ◽  
Run‐Run Kang ◽  
Kai‐Ge Chen ◽  
Kuan Liu ◽  
Zhuo Ma ◽  
...  
Keyword(s):  
Protective Effect ◽  
Mitochondrial Biogenesis ◽  
Cultured Neurons ◽  
Sirtuin 3 ◽  
Primary Cultured Neurons

β-Amyloid Upregulates Intracellular Clusterin but not Secretory Clusterin in Primary Cultured Neurons and APP Mice

2017 ◽  
Vol 14 (11) ◽  
Author(s):  
Ping Wang ◽  
Keliang Chen ◽  
Yuehua Gu ◽  
Qihao Guo ◽  
Zhen Hong ◽  
...  
Keyword(s):  
Cultured Neurons ◽  
Β Amyloid ◽  
Primary Cultured Neurons

815 Tyrosine phosphorylation of bit in rat primary cultured neurons

1997 ◽  
Vol 28 ◽  
pp. S104
Author(s):  
Hiroshi Ohnishi ◽  
Misae Kubota ◽  
Shin-Ichiro Sano
Keyword(s):  
Tyrosine Phosphorylation ◽  
Cultured Neurons ◽  
Primary Cultured Neurons

scholarly journals Doc2b Ca2+ binding site mutants enhance synaptic release at rest at the expense of sustained synaptic strength

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Quentin Bourgeois-Jaarsma ◽  
Matthijs Verhage ◽  
Alexander J. Groffen
Keyword(s):  
Binding Site ◽  
Neurotransmitter Release ◽  
Action Potentials ◽  
Synaptic Strength ◽  
Cultured Neurons ◽  
Loss Of Function ◽  
Short Term ◽  
Synaptic Release ◽  
Activated State ◽  
Primary Cultured Neurons

Abstract Communication between neurons involves presynaptic neurotransmitter release which can be evoked by action potentials or occur spontaneously as a result of stochastic vesicle fusion. The Ca2+-binding double C2 proteins Doc2a and –b were implicated in spontaneous and asynchronous evoked release, but the mechanism remains unclear. Here, we compared wildtype Doc2b with two Ca2+ binding site mutants named DN and 6A, previously classified as gain- and loss-of-function mutants. They carry the substitutions D218,220N or D163,218,220,303,357,359A respectively. We found that both mutants bound phospholipids at low Ca2+ concentrations and were membrane-associated in resting neurons, thus mimicking a Ca2+-activated state. Their overexpression in hippocampal primary cultured neurons had similar effects on spontaneous and evoked release, inducing high mEPSC frequencies and increased short-term depression. Together, these data suggest that the DN and 6A mutants both act as gain-of-function mutants at resting conditions.

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