Elevated levels of ΔFosB and RGS9 in striatum in Parkinson’s disease

[1]  H. Dohlman.  Regulators of G Protein Signaling (RGS Proteins) , 2002 .

[2]  M. Kelz,et al.  &Dgr;FosB: a molecular switch underlying long-term neural plasticity , 2000, Current opinion in neurology.

[3]  E. Nestler,et al.  Dopamine-receptor stimulation: biobehavioral and biochemical consequences , 2000, Trends in Neurosciences.

[4]  M. Andersson,et al.  Striatal fosB Expression Is Causally Linked with l -DOPA-Induced Abnormal Involuntary Movements and the Associated Upregulation of Striatal Prodynorphin mRNA in a Rat Model of Parkinson's Disease , 1999, Neurobiology of Disease.

[5]  D. Surmeier,et al.  Expression of the transcription factor ΔFosB in the brain controls sensitivity to cocaine , 1999, Nature.

[6]  M. Andersson,et al.  Changes in the regional and compartmental distribution of FosB- and JunB-like immunoreactivity induced in the dopamine-denervated rat striatum by acute or chronic L-DOPA treatment , 1999, Neuroscience.

[7]  N. Hiroi,et al.  Region‐specific induction of ΔFosB by repeated administration of typical versus atypical antipsychotic drugs , 1999, Synapse.

[8]  E. Nestler,et al.  Cloning and Characterization of RGS9-2: A Striatal-Enriched Alternatively Spliced Product of the RGS9 Gene , 1999, The Journal of Neuroscience.

[9]  A. Gilman,et al.  Mammalian RGS Proteins: Barbarians at the Gate* , 1998, The Journal of Biological Chemistry.

[10]  E. Nestler,et al.  Regulators of G-Protein Signaling (RGS) Proteins: Region-Specific Expression of Nine Subtypes in Rat Brain , 1997, The Journal of Neuroscience.

[11]  M. Greenberg,et al.  FosB mutant mice: loss of chronic cocaine induction of Fos-related proteins and heightened sensitivity to cocaine's psychomotor and rewarding effects. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[12]  A. Graybiel,et al.  Atypical and typical neuroleptic treatments induce distinct programs of transcription factor expression in the striatum , 1996, The Journal of comparative neurology.

[13]  E. Nestler,et al.  Chronic Alterations in Dopaminergic Neurotransmission Produce a Persistent Elevation of ΔFosB‐like Protein(s) in both the Rodent and Primate Striatum , 1996, The European journal of neuroscience.

[14]  F I Carroll,et al.  Mapping dopamine transporters in the human brain with novel selective cocaine analog [125I]RTI‐121 , 1995, Synapse.

[15]  David W. Self,et al.  Induction of a long-lasting AP-1 complex composed of altered Fos-like proteins in brain by chronic cocaine and other chronic treatments , 1994, Neuron.

[16]  T. Paolo,et al.  Long-term effects of MPTP on central and peripheral catecholamine and indoleamine concentrations in monkeys , 1986, Brain Research.

[17]  A. Rajput,et al.  Chronic low‐dose levodopa therapy in Parkinson's disease , 1984, Neurology.

[18]  G. Robertson,et al.  D1-Receptor-related priming is attenuated by antisense-meditated 'knockdown' of fosB expression. , 1998, Brain research. Molecular brain research.

[19]  J. Morgan,et al.  MPTP-Parkinsonism is accompanied by persistent expression of a delta-FosB-like protein in dopaminergic pathways. , 1998, Brain research. Molecular brain research.

[20]  S J Kish,et al.  Biochemical pathophysiology of Parkinson's disease. , 1987, Advances in neurology.