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Volume 17, Number 10,
Issue of May 15, 1997
pp. 3455-3466
Copyright ©1997 Society for Neuroscience
Glutamate, But Not Dopamine, Stimulates Stress-Activated Protein
Kinase and AP-1-Mediated Transcription in Striatal Neurons
Received Sept. 30, 1996; revised Feb. 26, 1997; accepted Feb. 28, 1997.
Michael A. Schwarzschild1, 2, ,
Rebecca L. Cole1, 4, , and
Steven E. Hyman1, 3, 4
1 Laboratory of Molecular and Developmental
Neuroscience, Massachusetts General Hospital, Charlestown,
Massachusetts 02129, Departments of 2 Neurology and
3 Psychiatry, Massachusetts General Hospital and Harvard
Medical School, Boston, Massachusetts 02115, and 4 Program
in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115
Drugs that stimulate dopamine and glutamate receptors have been
shown to induce the expression of AP-1 proteins (such as c-Fos and
c-Jun) in the striatum and to induce binding of these proteins to AP-1
sites on DNA, leading to the hypothesis that AP-1-mediated transcription contributes to the long-term effects of these drugs. To
examine this hypothesis, we compared the regulation of AP-1-mediated transcription to the inductions of AP-1-binding activity and genes encoding AP-1 proteins in primary cultures of striatal neurons. Although glutamate, dopamine, and forskolin (an activator of adenylate cyclase) all induce c-fos mRNA and AP-1 binding, we
found, surprisingly, that only glutamate induces transcription of a
transfected AP-1-driven fusion gene. To explore the basis for this
discrepancy, we investigated the possibility that the phosphorylation
of c-Jun may also be required for AP-1-mediated transcription in
striatal neurons. Glutamate, but neither dopamine nor forskolin, raises
the levels of phosphorylated c-Jun as well as the activity of a Jun
kinase (SAPK/JNK) in striatal cultures. Both the glutamatergic
induction of AP-1-mediated transcription and activation of SAPK/JNK
appear to be mediated, at least in part, via NMDA receptors. In
striatal neurons, the phosphorylation of AP-1 proteins produced by
glutamate may be required to convert AP-1 protein expression and
binding to transcriptional activation.
Key words:
glutamate;
NMDA;
SAPK;
JNK;
c-fos;
c-jun;
AP-1;
transcription;
striatum;
cell culture
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