Ascorbate transport by primary cultured neurons and its role in neuronal function and protection against excitotoxicity

2007 ◽  
Vol 85 (5) ◽  
pp. 1046-1056 ◽  
Author(s):  
Shenfeng Qiu ◽  
Liying Li ◽  
Edwin J. Weeber ◽  
James M. May
Keyword(s):  
Cultured Neurons ◽  
Neuronal Function ◽  
Ascorbate Transport ◽  
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.

Sign in / Sign up

Export Citation Format

Share Document