Lithium antagonizes dopamine-dependent behaviors mediated by an AKT/glycogen synthase kinase 3 signaling cascade.
By J. Beaulieu, T. Sotnikova, W. Yao, Lisa Kockeritz, J. Woodgett, R. Gainetdinov, M. Caron. Proceedings of the National Academy of Sciences of the United States of America, 2004
814 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/f0bc6142435a9e597ce42988371e05e1a31a6a28
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In Cellular and Molecular Neuroscience
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Citations in the corpus
- DISC1 regulates neural progenitor proliferation via modulation of GSK3β/β-catenin signaling (2009, background): “It was shown previously that genetic or pharmacological inhibition of GSK3b reduced amphetamine-induced hyperactivity in mice (Beaulieu et al., 2004), a model of mania-like behavior.”
- The Physiology, Signaling, and Pharmacology of Dopamine Receptors (2011, background): “Increased extracellular dopamine levels also result in an elevation in the level of ERK activity and in the development of a hyperactive phenotype in DAT-KO mice (Giros et al., 1996; Gainetdinov et al., 1999b; Beaulieu et al., 2004).”
- PI3K/Akt: getting it right matters (2008, background): “By interacting with the GSK3 pathway, Akt modulates the suppression of dopamine (DA)-associated behaviors after treatment with the mood stabilizer lithium (Beaulieu et al., 2004).”
- Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases (2014, background): “Most well-understood is the dopamine D2 receptor signaling mechanism that involves GSK3 and β-arrestin (Beaulieu et al., 2004; Beaulieu et al., 2005; Beaulieu et al., 2008).”