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Volume 8, Issue 1 (Suppl) J Cell Sci Ther
ISSN: 2157-7013 JCEST, an open access journal Stem Cell Research 2017
March 20-22, 2017
March 20-22, 2017 Orlando, USA
8th World Congress and Expo on
Cell & Stem Cell Research
Relationship between anesthetic-induced toxicity and NMDA receptor-mediated calcium influx in
developing neurons
Cheng Wang, Fang Liu, Tucker A Patterson, Merle G Paule and William Slikker
National Center for Toxicological Research/Food and Drug Administration, USA
Ketamine is a non-competitive NMDA receptor antagonist and is used as a general anesthetic. Recent data suggest that anesthetics
can cause neuronal damage when exposure occurs during development. To elucidate the underlying mechanisms associated
with ketamine neurotoxicity, neural cells were harvested from the forebrain of newborn rats and neural stem cells were isolated
from gestational day-16 rats. To determine the effect of ketamine on developing neurons and undifferentiated neural stem cells,
cultures were exposed to 10 µM ketamine for 24 hours. Ketamine exposure resulted in elevated NMDA receptor (NR1) expression in
primary cultures, and enhanced damage of developing neurons including those differentiated from the neural stem cells. However,
the viability and proliferation rate of neural stem cells were not significantly affected after ketamine exposure. Calcium imaging
data indicated that 50 µM NMDA did not cause a significant influx of calcium in typical neural stem cells; however, it has produced
an immediate elevation of intracellular free Ca2+ [Ca2+]i in neurons differentiated from the same neural stem cells. These findings
suggest that prolonged exposure of developing neurons to ketamine produces an increase in NMDA receptor expression, which
allows for a higher/toxic influx of calcium into neurons once ketamine is removed from the system, leading to neuronal cell death
likely due to elevated reactive oxygen species generation.
J Cell Sci Ther 2017, 8:1 (Suppl)