scholarly journals Concentration-Dependent Dual Role of Thrombin in Protection of Cultured Rat Cortical Neurons

2015 ◽  
Vol 40 (11) ◽  
pp. 2220-2229 ◽  
Author(s):  
Paul S. García ◽  
Vincent T. Ciavatta ◽  
Jonathan A. Fidler ◽  
Anna Woodbury ◽  
Jerrold H. Levy ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Dual Role ◽  
Rat Cortical Neurons

scholarly journals A dual role of EphB1/ephrin-B3 reverse signaling on migrating striatal and cortical neurons originating in the preoptic area: should I stay or go away?

2014 ◽  
Vol 8 ◽  
Author(s):  
Judith Rudolph ◽  
Katrin Gerstmann ◽  
Geraldine Zimmer ◽  
André Steinecke ◽  
Annika Döding ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Preoptic Area ◽  
Dual Role ◽  
Reverse Signaling

The dual role of KCNQ/M channels upon OGD or OGD/R insults in cultured cortical neurons of mice: Timing is crucial in targeting M‐channels against ischemic injur ies

2018 ◽  
Vol 234 (8) ◽  
pp. 12714-12726
Author(s):  
Yu Diao ◽  
Weijie Yan ◽  
Wei Sun ◽  
Yanlin Luo ◽  
Junfa Li ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Dual Role ◽  
Cultured Cortical Neurons ◽  
M Channels

scholarly journals Nckβ Adapter Controls Neuritogenesis by Maintaining the Cellular Paxillin Level

2007 ◽  
Vol 27 (17) ◽  
pp. 6001-6011 ◽  
Author(s):  
Shengxi Guan ◽  
Mei Chen ◽  
David Woodley ◽  
Wei Li
Keyword(s):  
Pc12 Cells ◽  
Cortical Neurons ◽  
State Level ◽  
Cell Types ◽  
Steady State Level ◽  
Down Regulation ◽  
Evolutionarily Conserved ◽  
Rat Cortical Neurons ◽  
Interfering Rna

ABSTRACT The SH2/SH3 adapter Nck has an evolutionarily conserved role in neurons, linking the cell surface signals to actin cytoskeleton-mediated responses. The mechanism, however, remains poorly understood. We have investigated the role of Nck/Nckα/Nck1 versus Grb4/Nckβ/Nck2 side-by-side in the process of mammalian neuritogenesis. Here we show that permanent genetic silencing of Nckβ, but not Nckα, completely blocked nerve growth factor-induced neurite outgrowth in PC12 cells and dramatically disrupted the axon and dendrite tree in primary rat cortical neurons. By screening for changes among the components reportedly present in complex with Nck, we found that the steady-state level of paxillin was significantly reduced in Nckβ knockdown, but not Nckα knockdown, neurons. Interestingly, Nckβ knockdown did not affect the paxillin level in glial cells and several other cell types of various tissue origins. Genetic silencing of paxillin blocked neuritogenesis, just like Nckβ knockdown. Reintroducing a nondegradable Nckβ into Nckβ short interfering RNA-expressing PC12 cells rescued paxillin from down-regulation and allowed the resumption of neuritogenesis. Forced expression of paxillin in Nckβ knockdown PC12 also rescued its capacity for neuritogenesis. Finally, Nckβ, but not Nckα, binds strongly to paxillin and treatment of the neurons with proteosome inhibitors prevented paxillin down-regulation in Nckβ knockdown neurons. Thus, Nckβ maintains paxillin stability during neuritogenesis.

A Role of Peroxides in Ca2+Ionophore-Induced Apoptosis in Cultured Rat Cortical Neurons

1996 ◽  
Vol 227 (2) ◽  
pp. 513-518 ◽  
Author(s):  
Yutaka Hatanaka ◽  
Keiichiro Suzuki ◽  
Yoshimi Kawasaki ◽  
Yasuhisa Endo ◽  
Naoyuki Taniguchi ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Rat Cortical Neurons ◽  
Induced Apoptosis

Axonal fasciculation and the role of polysialic acid-neural cell adhesion molecule in rat cortical neurons

2013 ◽  
Vol 91 (11) ◽  
pp. 1408-1418 ◽  
Author(s):  
Chandramohan G. Wakade ◽  
Shyamal H. Mehta ◽  
Manebu Maeda ◽  
R. Clinton Webb ◽  
Fung-Chow Chiu
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cortical Neurons ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Polysialic Acid ◽  
Neural Cell ◽  
Neural Cell Adhesion ◽  
Rat Cortical Neurons

Cellular levels of TrkB and MAPK in the neuroprotective role of BDNF for embryonic rat cortical neurons against hypoxia in vitro

2005 ◽  
Vol 23 (6) ◽  
pp. 515-521 ◽  
Author(s):  
Mao Meng ◽  
Wang Zhiling ◽  
Zhou Hui ◽  
Li Shengfu ◽  
Yu Dan ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Rat Cortical Neurons

scholarly journals Calcium Export from Neurons and Multi-Kinase Signaling Cascades Contribute to Ouabain Neuroprotection in Hyperhomocysteinemia

Biomolecules ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1104
Author(s):  
Maria A. Ivanova ◽  
Arina D. Kokorina ◽  
Polina D. Timofeeva ◽  
Tatiana V. Karelina ◽  
Polina A. Abushik ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Primary Cultures ◽  
Glutamate Excitotoxicity ◽  
Neuroprotective Effects ◽  
Mediated Effects ◽  
Mitochondrial Inner Membrane ◽  
Rat Cortical Neurons ◽  
Proteinkinase C ◽  
Apoptosis Related Protein

Pathological homocysteine (HCY) accumulation in the human plasma, known as hyperhomocysteinemia, exacerbates neurodegenerative diseases because, in the brain, this amino acid acts as a persistent N-methyl-d-aspartate receptor agonist. We studied the effects of 0.1–1 nM ouabain on intracellular Ca2+ signaling, mitochondrial inner membrane voltage (φmit), and cell viability in primary cultures of rat cortical neurons in glutamate and HCY neurotoxic insults. In addition, apoptosis-related protein expression and the involvement of some kinases in ouabain-mediated effects were evaluated. In short insults, HCY was less potent than glutamate as a neurotoxic agent and induced a 20% loss of φmit, whereas glutamate caused a 70% decrease of this value. Subnanomolar ouabain exhibited immediate and postponed neuroprotective effects on neurons. (1) Ouabain rapidly reduced the Ca2+ overload of neurons and loss of φmit evoked by glutamate and HCY that rescued neurons in short insults. (2) In prolonged 24 h excitotoxic insults, ouabain prevented neuronal apoptosis, triggering proteinkinase A and proteinkinase C dependent intracellular neuroprotective cascades for HCY, but not for glutamate. We, therefore, demonstrated here the role of PKC and PKA involving pathways in neuronal survival caused by ouabain in hyperhomocysteinemia, which suggests existence of different appropriate pharmacological treatment for hyperhomocysteinemia and glutamate excitotoxicity.

Cannabis-like activity of Zornia latifolia Sm. detected in vitro on rat cortical neurons: major role of the flavone syzalterin

2020 ◽  
pp. 1-13
Author(s):  
Susanna Alloisio ◽  
Marco Clericuzio ◽  
Mario Nobile ◽  
Annalisa Salis ◽  
Gianluca Damonte ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Rat Cortical Neurons

scholarly journals Desensitization of NMDA receptors depends of their association with plasma membrane sodium-calcium exchangers in lipid nanoclasters

2018 ◽  
Author(s):  
Dmitry A. Sibarov ◽  
Ekaterina E. Poguzhelskaya ◽  
Sergei M. Antonov
Keyword(s):  
Plasma Membrane ◽  
Steady State ◽  
Cortical Neurons ◽  
External Solution ◽  
Membrane Lipid ◽  
Before And After ◽  
Rat Cortical Neurons ◽  
Amplitude Decrease

AbstractThe plasma membrane Na+/Ca2+-exchanger (NCX) has recently been shown to regulate Ca2+-dependent N-methyl-d-aspartate receptor (NMDAR) desensitization, suggesting tight interaction of NCXs and NMDARs in lipid nanoclaster or “rafts”. To evaluate possible role of this interaction we studied effects of Li+ on NMDA-elicited whole-cell currents and Ca2+ responses of rat cortical neurons in vitro before and after cholesterol extraction by methyl-β-cyclodextrin (MβCD). Substitution Li+ for Na+ in the external solution caused a concentration-dependent decrease of steady-state NMDAR currents from 440 ± 71 pA to 111 ± 29 pA in 140 mM Na+ and 140 mM Li+, respectively. Li+ inhibition of NMDAR currents disappeared in the absence of Ca2+ in the external solution (Ca2+-free), suggesting that Li+ enhanced Ca2+-dependent NMDAR desensitization. Whereas the cholesterol extraction with MβCD induced NMDAR current decrease to 136 ± 32 pA in 140 mM Na+ and 46 ± 15 pA in 140 mM Li+, the IC50 values for the Li+ inhibition were similar (about 44 mM Li+) before and after this procedure. In Ca2+-free Na+ solution steady-state NMDAR currents after the cholesterol extraction were 47 ± 6 % of control currents. Apparently this amplitude decrease was not Ca2+-dependent. In 1 mM Ca2+ Na+ solution the Ca2+-dependent NMDAR desensitization was greater when cholesterol was extracted. Obviously, this procedure promoted its development. In agreement, Li+ and KB-R7943, an inhibitor of NCX, both considerably reduced NMDAR-mediated Ca2+ responses. The cholesterol extraction itself caused a decrease of NMDAR-mediated Ca2+ responses and, in addition, abolished the effects of Li+ and KB-R7943. Taken together our data suggest that NCXs downregulate the Ca2+-dependent NMDAR desensitization. Most likely, this is determined by co-localization and tight functional interaction of NCX and NMDAR molecules in membrane lipid rafts. Their destruction is accompanied by an enhancement of NMDAR desensitization and a loss of NCX-selective agent effects on NMDARs.

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