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J. Biol. Chem., Vol. 276, Issue 34, 31674-31683, August 24, 2001
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From the The mood-stabilizing agents lithium and valproic
acid (VPA) increase DNA binding activity and transactivation activity
of AP-1 transcription factors, as well as the expression of genes regulated by AP-1, in cultured cells and brain regions involved in mood
regulation. In the present study, we found that VPA activated extracellular signal-regulated kinase (ERK), a kinase known to regulate AP-1 function and utilized by neurotrophins to mediate their diverse effects, including neuronal differentiation,
neuronal survival, long term neuroplasticity, and potentially learning and memory. VPA-induced activation of ERK was blocked by the
mitogen-activated protein kinase/ERK kinase inhibitor
PD098059 and dominant-negative Ras and Raf mutants but
not by dominant-negative stress-activated protein kinase/ERK kinase and
mitogen-activated protein kinase kinase 6 mutants. VPA also
increased the expression of genes regulated by the ERK pathway,
including growth cone-associated protein 43 and Bcl-2, promoted
neurite growth and cell survival, and enhanced norepinephrine uptake
and release. These data demonstrate that VPA is an ERK pathway
activator and produces neurotrophic effects.
The Mood Stabilizer Valproic Acid Activates Mitogen-activated
Protein Kinases and Promotes Neurite Growth*
,,,¶, and¶
Laboratory of Molecular Pathophysiology,
Department of Psychiatry and Behavioral Neurosciences, Wayne State
University School of Medicine, Detroit, Michigan 48201, the
§ Oral and Pharyngeal Cancer Branch, NIDCR, National
Institutes of Health, Bethesda, Maryland 20892, and the
¶ Laboratory of Molecular Pathophysiology, National Institute of
Mental Health, Bethesda, Maryland 20892
*
This work was supported by National Institute of Health
Grant MH57743 (to H. K. M.), the Joe Young Senior Research Fund, and the Theodore and Vada Stanley Foundation.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Unit on Molecular
Neurotherapeutics, Laboratory of Molecular Pathophysiology, NIMH, NIH,
Bldg. 49, Rm. B1EE16, 49 Convent Drive, MSC 4405, Bethesda, MD 20892-4405. Tel.: 301-496-9802; Fax: 301-480-0123;
E-mail: gchen@codon.nih.gov.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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