Lithium blocks ethanol-induced modulation of protein kinases in the developing brain

Biochemical and Biophysical Research Communications
Goutam ChakrabortyMariko Saito

Abstract

Lithium has been shown to be neuroprotective against various insults including ethanol exposure. We previously reported that ethanol-induced apoptotic neurodegeneration in the postnatal day 7 (P7) mice is associated with decreases in phosphorylation levels of Akt, glycogen synthase kinase-3beta (GSK-3beta), and AMP-activated protein kinase (AMPK), and alteration in lipid profiles in the brain. Here, P7 mice were injected with ethanol and lithium, and the effects of lithium on ethanol-induced alterations in phosphorylation levels of protein kinases and lipid profiles in the brain were examined. Immunoblot and immunohistochemical analyses showed that lithium significantly blocked ethanol-induced caspase-3 activation and reduction in phosphorylation levels of Akt, GSK-3beta, and AMPK. Further, lithium inhibited accumulation of cholesterol ester (ChE) and N-acylphosphatidylethanolamine (NAPE) triggered by ethanol in the brain. These results suggest that Akt, GSK-3beta, and AMPK are involved in ethanol-induced neurodegeneration and the neuroprotective effects of lithium by modulating both apoptotic and survival pathways.

References

Aug 6, 1996·Proceedings of the National Academy of Sciences of the United States of America·P S Klein, D A Melton
Jul 21, 1999·Proceedings of the National Academy of Sciences of the United States of America·E Chalecka-Franaszek, D M Chuang
Mar 8, 2002·Brain Research. Developmental Brain Research·John W OlneyChrysanthy Ikonomidou
Jun 20, 2002·Bipolar Disorders·Xiaohua LiRichard S Jope
Apr 18, 2003·The Journal of Biological Chemistry·Julia XuSuzanne de la Monte
Sep 23, 2003·Cell Death and Differentiation·C YoungJ W Olney
Jun 2, 2005·Neurobiology of Disease·Chainllie YoungJohn W Olney
Apr 29, 2006·The Journal of Physiology·D Grahame HardieJohn W Scott
Oct 19, 2006·Biochemical and Biophysical Research Communications·Jin ZhongWeihua Lee
Jan 27, 2007·The Journal of Biological Chemistry·Yong WuMing-Hui Zou
Mar 22, 2007·Alcoholism, Clinical and Experimental Research·Mariko SaitoMitsuo Saito
Apr 5, 2007·Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology·Kaan YucelGlenda M MacQueen
Jul 3, 2007·Cell·Brendan D Manning, Lewis C Cantley
Oct 26, 2007·The Journal of Biological Chemistry·Gawain McCollGordon J Lithgow

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Citations

Jun 10, 2009·Molecular Neurobiology·Jia Luo
Jan 10, 2013·Pharmacological Reviews·Chi-Tso ChiuDe-Maw Chuang
Apr 12, 2013·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Shivakumar SubbannaBalapal S Basavarajappa
May 26, 2011·Neurotoxicology and Teratology·Renata da Luz OliveiraCarla Denise Bonan
Aug 2, 2008·Neuroscience Letters·Tania F GendronShu-Hui Yen
Sep 25, 2012·Biochimica Et Biophysica Acta·Niels WellnerHarald Severin Hansen
Aug 19, 2016·Brain Sciences·Mariko SaitoMitsuo Saito
Apr 11, 2009·The Neuroscientist : a Review Journal Bringing Neurobiology, Neurology and Psychiatry·Milos R SpasićKoenraad K Norga
Jun 16, 2009·Cell Transplantation·Wise Young
Feb 26, 2016·Bulletin of Experimental Biology and Medicine·P N MenshanovN N Dygalo
Mar 1, 2012·Neuromolecular Medicine·Zhiyou CaiBin Zhao
Sep 13, 2013·Brain Sciences·Benjamin SadrianMariko Saito
Jan 1, 2013·Brain Sciences·Mariko Saito, Mitsuo Saito

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis