Cocaine and the AP-1 transcription factor complex

Annals of the New York Academy of Sciences

Volumn 844, Issue , 1998, Pages 1-6

  Hope, Bruch T ^a  

^a NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

COCAINE; PROTEIN C FOS; TRANSCRIPTION FACTOR AP 1;

AMINO ACID SEQUENCE; CONFERENCE PAPER; CORPUS STRIATUM; DRUG DEPENDENCE; GENE EXPRESSION; GENE INDUCTION; HUMAN; IMMEDIATE EARLY GENE; NERVE CELL PLASTICITY; NONHUMAN; NUCLEUS ACCUMBENS; ONCOGENE C FOS; PROTEIN DOMAIN; PROTEIN PURIFICATION; TRANSCRIPTION INITIATION;

ANIMALIA;

EID: 0031847127     PISSN: 00778923     EISSN: None     Source Type: Book Series    
DOI: 10.1111/j.1749-6632.1998.tb08216.x     Document Type: Conference Paper

References (29)

1. KOOB, G.F. & F.E. BLOOM. 1988. Cellular and molecular mechanisms of drug dependence. Science 242: 715-723.
2. NESTLER, E.J., B.T. HOPE & K.L. WIDNELL. 1993. Drug addiction: A model for the molecular basis of neural plasticity. Neuron 11: 995-1006.
3. SELF, D.W. & E.J. NESTLER. 1995. Molecular mechanisms of drug reinforcement and addiction. Annu. Rev. Neurosci. 18: 463-495.
4. GAWIN, F.H. 1991. Cocaine addiction: psychology and neurophysiology. Science 251: 1580-1586.
5. HYMAN, S.E. & E.J. NESTLER. 1993. The Molecular Basis of Psychiatry. American Psychiatric Press. Washington.
6. EDWARDS, D.R. 1994. Cell signalling and the control of gene transcription. Trends Pharmacol. Sci. 15:239-244.
7. TJIAN, R. 1995. Molecular machines that control genes. Sci. Am. 272: 54-61.
8. MORGAN J.I. & T. CURRAN. 1991. Stimulus-transcription coupling in the nervous system: Involvement of the inducible protooncogenes fos and jun. Annu. Rev. Neurosci. 14: 421-451.
9. GRAYBIEL, A.M., R. MORATALLA & H.A. ROBERTSON. 1990. Amphetamine and cocaine induce drug-specific activation of the c-fos gene in striosome-matrix compartments and limbic subdivisions of the striatum. Proc. Natl. Acad. Sci. USA 87: 6912-6916.
10. 1 receptors. Proc. Natl. Acad. Sci. USA 88: 1291-1295.
11. HOPE, B.T., B. KOSOFSKY, S.E. HYMAN & E.J. NESTLER. 1992. Regulation of immediate early gene expression and AP-1 binding in the rat nucleus accumbens by chronic cocaine. Proc. Natl. Acad. Sci. USA 89: 5764-5768.
12. ENNULAT, D.J., S.M. BABB & B.M. COHEN. 1994. Persistent reduction of immediate early gene mRNA in rat forebrain following single and multiple doses of cocaine. Mol. Brain Res. 26: 106-112.
13. COLE, R.L., C. KONRADI, J. DOUGLASS & S.E. HYMAN. 1995. Neuronal adaptation to amphetamine and dopamine: Molecular mechanisms of prodynorphin gene regulation in rat striatum. Neuron 14: 813-823.
14. STEINER, H. & C.R. GERFEN. 1993. Cocaine-induced c-fos messenger RNA is inversely related to dynorphin expression in striatum. J. Neurosci. 13: 5066-5081.
15. SIVAM, S.P. 1989. Cocaine selectively increases striatonigral dynorphin levels by a dopaminergic mechanism. J. Pharmacol. Exp. Then 256: 818-824.
16. DAUNAIS, J.B. & J.F. MCGINTY. 1994. Acute and chronic cocaine administration differentially alters striatal opioid and nuclear transcription factor mRNAs. Synapse 18: 35-45.
17. HOPE, B.T., H.E. NYE, M.B. KELZ, D.W. SELF, M.J. IADAROLA, Y. NAKABEPPU, R.S. DUMAN & E.J. NESTLER. 1994. Induction of a long-lasting AP-1 complex composed of altered Fos-like proteins in brain following chronic cocaine and other chronic treatments. Neuron 13: 1235-1244.
18. HOPE, B.T., M.B. KELZ, R.S. DUMAN & E.J. NESTLER. 1994. Chronic electroconvulsive seizure (ECS) treatment results in expression of a long-lasting AP-1 complex in brain with altered composition and characteristics. J. Neurosci. 14:4318-4328.
19. NYE, H.E., B.T. HOPE, M.B. KELZ, M. IADAROLA & E.J. NESTLER. 1995. Pharmacological studies of the regulation of chronic FOS-related antigen induction by cocaine in the striatum and nucleus accumbens. J. Pharmacol. Exp. Therap. 275: 1671-1680.
20. PENNYPACKER, K.R., L. THAI, J.-S. HONG & M.K. MCMILLIAN. 1994. Prolonged expression of AP-1 transcription factors in the rat hippocampus after systemic kainate treatment. J. Neurosci. 14: 3998-4006.
21. CHEN, J.-S, H.E. NYE, M.B. KELZ, N. HIROI, Y. NAKABEPPU, B.T. HOPE & E.J. NESTLER. 1995. Regulation of delta FosB and FosB-like proteins by electroconvulsive seizure and cocaine treatments. Mol. Pharmacol. 48: 880-889.
22. DOUCET, J.-P., Y. NAKABEPPU, P.J. BEDARD, B.T. HOPE, E.J. NESTLER, B.J. JASMIN, J.-S. CHEN, M.J. IADAROLA, M. ST-JEAN, N. WIGLE, P. BLANCHET, R. GRONDIN & G.S. ROBERTSON. 1996. Chronic alterations in dopaminergic neurotransmission produce a persistent elevation of delta FosB-like protein(s) in both the rodent and primate striatum. Eur. J. Neurosci. 8: 365-381.
23. MANDELZYS, A., M.A. GRUDA, R. BRAVO & J. MORGAN. 1997. Absence of a persistently elevated 37 kDa Fos-related antigen and AP-1-like DNA-binding activity in the brains of kainic acid-treated fosB null mice. J. Neurosci. 17: 5407-5415.
24. HIROI, R, J.R. BROWN, C.N. HAILE, H. YE, M.E. GREENBERG & E.J. NESTLER. 1997. FosB mutant mice: Loss of chronic cocaine induction of Fos-related proteins and heightened sensitivity to cocaine's psychomotor and rewarding effects. Proc. Natl. Acad. Sci. USA 94: 10397-10402.
25. NAKABEPPU, Y. & D. NATHANS. 1991. A naturally occurring truncated form of FosB that inhibits Fos/Jun transcriptional activity. Cell 64: 751-759.
26. YEN, J., R.M. WISDOM, I. TRATNER & I. VERMA. 1991. An alternative spliced form of FosB is a negative regulator of transcriptional activation and transformation by Fos proteins. Proc. Natl. Acad. Sci. USA 88: 5077-5081.
27. DOBRZANSKI, P., T. NOGUCHI, K. KOVARY, C.A. RIZZO, P.S. LAZO & R. BRAVO. 1991. Both products of the fosB gene, FosB and its short form, FosB/SF, are transcriptional activators in fibroblasts. Mol. Cell. Biol. 11: 5470-5478.
28. MUMBERG, D., F.C. LUCIBELLO, M. SCHUERMANN & R. MULLER. 1991. Alternative splicing of fosB transcripts results in differentially expressed mRNAs encoding functionally antagonistic proteins. Genes Dev. 5: 1212-1223.
29. HIRAI, S.-I., R.-P. RYSECK, F. MECHTA, R. BRAVO & M. YANIV. 1989. Characterization of junD: A new member of the jun proto-oncogene family. EMBO J. 8: 1433-1439.