AUTHOR=Madji Hounoum Blandine , Vourc’h Patrick , Felix Romain , Corcia Philippe , Patin Franck , Guéguinou Maxime , Potier-Cartereau Marie , Vandier Christophe , Raoul Cédric , Andres Christian R. , Mavel Sylvie , Blasco Hélène 

TITLE=NSC-34 Motor Neuron-Like Cells Are Unsuitable as Experimental Model for Glutamate-Mediated Excitotoxicity

JOURNAL=Frontiers in Cellular Neuroscience

VOLUME=10

YEAR=2016

URL=https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2016.00118

DOI=10.3389/fncel.2016.00118

ISSN=1662-5102

ABSTRACT=<p>Glutamate-induced excitotoxicity is a major contributor to motor neuron degeneration in the pathogenesis of amyotrophic lateral sclerosis (ALS). The spinal cord × Neuroblastoma hybrid cell line (NSC-34) is often used as a<italic> bona fide</italic> cellular model to investigate the physiopathological mechanisms of ALS. However, the physiological response of NSC-34 to glutamate remains insufficiently described. In this study, we evaluated the relevance of differentiated NSC-34 (NSC-34<sub>D</sub>) as an <italic>in vitro</italic> model for glutamate excitotoxicity studies. NSC-34<sub>D</sub> showed morphological and physiological properties of motor neuron-like cells and expressed glutamate receptor subunits GluA1–4, GluN1 and GluN2A/D. Despite these diverse characteristics, no specific effect of glutamate was observed on cultured NSC-34<sub>D</sub> survival and morphology, in contrast to what has been described in primary culture of motor neurons (MN). Moreover, a small non sustained increase in the concentration of intracellular calcium was observed in NSC-34<sub>D</sub> after exposure to glutamate compared to primary MN. Our findings, together with the inability to obtain cultures containing only differentiated cells, suggest that the motor neuron-like NSC-34 cell line is not a suitable <italic>in vitro</italic> model to study glutamate-induced excitotoxicity. We suggest that the use of primary cultures of MN is more suitable than NSC-34 cell line to explore the pathogenesis of glutamate-mediated excitotoxicity at the cellular level in ALS and other motor neuron diseases.</p>