Ketamine-induced apoptosis in cultured rat cortical neurons
by
Takadera T, Ishida A, Ohyashiki T.
Department of Clinical Chemistry,
Faculty of Pharmaceutical Sciences,
Hokuriku University, Kanazawa 920-1148, Japan.
t-takadera@hokuriku-u.ac.jp
Toxicol Appl Pharmacol. 2006 Jan 1;210(1-2):100-7.


ABSTRACT

Recent data suggest that anesthetic drugs cause neurodegeneration during development. Ketamine is frequently used in infants and toddlers for elective surgeries. The purpose of this study is to determine whether glycogen synthase kinase-3 (GSK-3) is involved in ketamine-induced apoptosis. Ketamine increased apoptotic cell death with morphological changes which were characterized by cell shrinkage, nuclear condensation or fragmentation. In addition, insulin growth factor-1 completely blocked the ketamine-induced apoptotic cell death. Ketamine decreased Akt phosphorylation. GSK-3 is known as a downstream target of Akt. The selective inhibitors of GSK-3 prevented the ketamine-induced apoptosis. Moreover, caspase-3 activation was accompanied by the ketamine-induced cell death and inhibited by the GSK-3 inhibitors. These results suggest that activation of GSK-3 is involved in ketamine-induced apoptosis in rat cortical neurons.

Ketamine
Ketamine and memory
Ketamine and the nucleus accumbens
Ketamine: medical and non-medical use
The role of ketamine in pain management
Low-dose ketamine as a fast-onset, long-acting antidepressant


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