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Loss of the serum response factor in the dopaminesystem leads to hyperactivity
German Cancer Research Center, Heidelberg, Germany.
Central Institute of Mental Health,.
German Cancer Research Center, Heidelberg, Germany.
Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.
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2010 (English)In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 24, 2427-2435 p.Article in journal (Refereed) Published
Abstract [en]

The serum response factor (SRF) is a key regulator of neural development and cellular plasticity, which enables it to act as a regulator of long-term adaptations in neurons. Here we performed a comprehensive analysis of SRF function in the murine dopamine system. We found that loss of SRF in dopaminoceptive, but not dopaminergic, neurons is responsible for the development of a hyperactivity syndrome, characterized by reduced body weight into adulthood, enhanced motor activity, and deficits in habituation processes. Most important, the hyperactivity also develops when the ablation of SRF is induced in adult animals. On the molecular level, the loss of SRF in dopaminoceptive cells is associated with altered expression of neuronal plasticity-related genes, in particular transcripts involved in calcium ion binding, formation of the cytoskeleton, and transcripts encoding neuropeptide precursors. Furthermore, abrogation of SRF causes specific deficits in activity-dependent transcription, especially a complete lack of psychostimulant-induced expression of the Egr   genes. We inferred that alterations in SRFdependent  gene expression underlie the observed hyperactive behavior. Thus, SRF depletion in dopaminoceptive neurons might trigger molecular mechanisms responsible for development of psychopathological conditions involving hyperactivity.

Place, publisher, year, edition, pages
Federation of American Societies for Experimental Biology , 2010. Vol. 24, 2427-2435 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-65545DOI: 10.1096/fj.09-151423OAI: diva2:396666
Available from: 2011-02-10 Created: 2011-02-10 Last updated: 2011-02-11

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Engblom, David
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