Involvement of BDNF/ERK signaling in spontaneous recovery from trimethyltin-induced hippocampal neurotoxicity in mice

Brain Research Bulletin
Sueun LeeChangjong Moon

Abstract

Trimethyltin (TMT) toxicity causes histopathological damage in the hippocampus and induces seizure behaviors in mice. The lesions and symptoms recover spontaneously over time; however, little is known about the precise mechanisms underlying this recovery from TMT toxicity. We investigated changes in the brain-derived neurotrophic factor/extracellular signal-regulated kinases (BDNF/ERK) signaling pathways in the mouse hippocampus following TMT toxicity. Mice (7 weeks old, C57BL/6) administered TMT (2.6 mg/kg intraperitoneally) showed acute and severe neurodegeneration with increased TUNEL-positive cells in the dentate gyrus (DG) of the hippocampus. The mRNA and protein levels of BDNF in the hippocampus were elevated by TMT treatment. Immunohistochemical analysis showed that TMT treatment markedly increased phosphorylated ERK1/2 expression in the mouse hippocampus 1-4 days after TMT treatment, although the intensity of ERK immunoreactivity in mossy fiber decreased at 1-8 days post-treatment. In addition, ERK-immunopositive cells were localized predominantly in doublecortin-positive immature progenitor neurons in the DG. In primary cultured immature hippocampal neurons (4 days in vitro), BDNF treatment alleviated TMT-induced neuro...Continue Reading

References

Jun 1, 1987·Neurology·R BesserH C Hopf
Jan 1, 1996·Annual Review of Neuroscience·R A Segal, M E Greenberg
Oct 6, 1999·Current Opinion in Neurobiology·S S GrewalP J Stork
Oct 27, 1999·Proceedings of the National Academy of Sciences of the United States of America·A AlessandriniJ V Bonventre
Feb 16, 2002·Methods : a Companion to Methods in Enzymology·K J Livak, T D Schmittgen
Oct 3, 2002·The EMBO Journal·Josefina GarciaFrançoise Porteu
Apr 28, 2004·Neurotoxicity Research·G Jean HarryChristian Lefebvre d'Hellencourt
May 22, 2004·European Journal of Biochemistry·Michal Hetman, Agata Gozdz
Dec 24, 2004·Journal of Cell Science·Mi-Sun YunKang-Yell Choi
Feb 18, 2005·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Ursula SchenkMichela Matteoli
Jun 20, 2006·The Journal of Pharmacology and Experimental Therapeutics·Jun MatsumotoJun-ichi Kuratsu
Sep 4, 2007·Progress in Brain Research·David B Jaffe, Rafael Gutiérrez
Jan 22, 2008·Nature Neuroscience·Tomoya MatsumotoYves-Alain Barde
Jun 3, 2009·Proceedings of the National Academy of Sciences of the United States of America·Hugo VaraMaurizio Giustetto
Jan 20, 2011·Proceedings of the National Academy of Sciences of the United States of America·Carlos SindreuDaniel R Storm
Mar 19, 2011·Neurochemistry International·Maria Concetta GelosoFabrizio Michetti
Apr 1, 2011·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Cory A BlaissSteven G Kernie
Apr 5, 2011·Biochemical Pharmacology·Miyoung YangChangjong Moon
May 3, 2011·Trends in Biochemical Sciences·Michelle C MendozaJohn Blenis

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Citations

Jan 12, 2019·Neural Regeneration Research·Wen-Bo ZhouBin Yu
Jul 10, 2021·Journal of Neuroinflammation·Giuseppe GalvaniStefania Trazzi

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