scholarly journals Neurotensin Enhances Endogenous Extracellular Glutamate Levels in Primary Cultures of Rat Cortical Neurons: Involvement of Neurotensin Receptor in NMDA Induced Excitotoxicity

2004 ◽  
Vol 14 (4) ◽  
pp. 466-473 ◽  
Author(s):  
T. Antonelli
Keyword(s):  
Cortical Neurons ◽  
Primary Cultures ◽  
Extracellular Glutamate ◽  
Neurotensin Receptor ◽  
Rat Cortical Neurons

scholarly journals Inhibition of cPLA2 and sPLA2 Activities in Primary Cultures of Rat Cortical Neurons by Centella asiatica Water Extract

2012 ◽  
Vol 7 (7) ◽  
pp. 1934578X1200700 ◽  
Author(s):  
Patrícia P. Defillipo ◽  
André H. Raposo ◽  
Alessandra G. Fedoce ◽  
Aline S. Ferreira ◽  
Hudson C. Polonini ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Leaf Extract ◽  
Primary Cultures ◽  
Water Extract ◽  
Centella Asiatica ◽  
Long Time ◽  
Rat Cortical Neurons ◽  
Low Toxicity ◽  
The Brain

Leaf extract of Centella asiatica has been used as an alternative medicine for memory improvement in the Indian Ayurvedic system of medicine for a long time. Although several studies have revealed its effect in ameliorating the cognitive impairment in rat models of Alzheimer's disease, the molecular mechanism of C. asiatica on neuroprotection still remains unexplained. In this study, we investigated the effects of C. asiatica water extract on activity of subtypes of phospholipase A2 (PLA2) in primary cultures of rat cortical neurons and quantified by HPLC a possible molecule responsible for the activity. The cPLA2 and sPLA2 activities were inhibited in vitro by asiaticoside present in the water extract of C. asiatica. This extract may be a candidate for the treatment of neurodegenerative processes because of its pharmacological activity in the brain and its low toxicity, as attested by its long popular use as a natural product.

scholarly journals Comparative Proteomics Unveils LRRFIP1 as a New Player in the DAPK1 Interactome of Neurons Exposed to Oxygen and Glucose Deprivation

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1202
Author(s):  
Núria DeGregorio-Rocasolano ◽  
Verónica Guirao ◽  
Jovita Ponce ◽  
Marc Melià-Sorolla ◽  
Alicia Aliena-Valero ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Primary Cultures ◽  
Lipid Peroxides ◽  
Glucose Deprivation ◽  
Redox Status ◽  
Protein Levels ◽  
Neuronal Fate ◽  
Death Associated Protein Kinase ◽  
Rat Cortical Neurons

Death-associated protein kinase 1 (DAPK1) is a pleiotropic hub of a number of networked distributed intracellular processes. Among them, DAPK1 is known to interact with the excitotoxicity driver NMDA receptor (NMDAR), and in sudden pathophysiological conditions of the brain, e.g., stroke, several lines of evidence link DAPK1 with the transduction of glutamate-induced events that determine neuronal fate. In turn, DAPK1 expression and activity are known to be affected by the redox status of the cell. To delineate specific and differential neuronal DAPK1 interactors in stroke-like conditions in vitro, we exposed primary cultures of rat cortical neurons to oxygen/glucose deprivation (OGD), a condition that increases reactive oxygen species (ROS) and lipid peroxides. OGD or control samples were co-immunoprecipitated separately, trypsin-digested, and proteins in the interactome identified by high-resolution LC-MS/MS. Data were processed and curated using bioinformatics tools. OGD increased total DAPK1 protein levels, cleavage into shorter isoforms, and dephosphorylation to render the active DAPK1 form. The DAPK1 interactome comprises some 600 proteins, mostly involving binding, catalytic and structural molecular functions. OGD up-regulated 190 and down-regulated 192 candidate DAPK1-interacting proteins. Some differentially up-regulated interactors related to NMDAR were validated by WB. In addition, a novel differential DAPK1 partner, LRRFIP1, was further confirmed by reverse Co-IP. Furthermore, LRRFIP1 levels were increased by pro-oxidant conditions such as ODG or the ferroptosis inducer erastin. The present study identifies novel partners of DAPK1, such as LRRFIP1, which are suitable as targets for neuroprotection.

Modulation of phospholipase A2 activity in primary cultures of rat cortical neurons

2005 ◽  
Vol 112 (10) ◽  
pp. 1297-1308 ◽  
Author(s):  
C. T. Mendes ◽  
W. F. Gattaz ◽  
E. L. Schaeffer ◽  
O. V. Forlenza
Keyword(s):  
Phospholipase A2 ◽  
Cortical Neurons ◽  
Primary Cultures ◽  
Rat Cortical Neurons ◽  
Phospholipase A2 Activity

Effects of triiodothyronine (T3) on differentiation of rat cortical neurons in primary cultures

1991 ◽  
Vol 5 (S1) ◽  
pp. 168-171 ◽  
Author(s):  
A. Cestelli ◽  
D. Castiglia ◽  
C. Di Liegro ◽  
L. Bonfanti ◽  
I. Di Liegro
Keyword(s):  
Cortical Neurons ◽  
Primary Cultures ◽  
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.

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