NDLI: Histone H3 phosphorylation is under the opposite tonic control of dopamine D2 and adenosine A2A receptors in striatopallidal neurons

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Histone H3 phosphorylation is under the opposite tonic control of dopamine D2 and adenosine A2A receptors in striatopallidal neurons

Content Provider	PubMed Central
Author	Jesus, Bertran-gonzalez Håkansson, Kerstin Anders, Borgkvist Irinopoulou, Theano Karen, Brami-cherrier Alessandro, Usiello Greengard, Paul Hervé, Denis Girault, Jean-antoine Valjent, Emmanuel Gilberto, Fisone
Abstract	The antipsychotic agent haloperidol regulates gene transcription in striatal medium spiny neurons (MSNs) by blocking dopamine D2 receptors (D2Rs). We examined the mechanisms by which haloperidol increases the phosphorylation of histone H3, a key step in nucleosomal response. Using BAC-transgenic mice that express EGFP under the control of the promoter of the dopamine D1 receptor or the D2R, we found that haloperidol induced a rapid and sustained increase in the phosphorylation of histone H3 in the striatopallidal MSNs of the dorsal striatum, with no change in its acetylation. This effect was mimicked by raclopride, a selective D2R-antagonist, and prevented by blockade of adenosine A2A receptors (A2ARs) or genetic attenuation of the A2AR-associated G protein, Gαolf. Mutation of the cAMP-dependent phosphorylation site (Thr34) of the 32-kDa dopamine- and cAMP-regulated phosphoprotein (DARPP-32) decreased haloperidol-induced H3 phosphorylation, supporting the role of cAMP in H3 phosphorylation. Haloperidol also induced extracellular signal-regulated kinase (ERK) phosphorylation in striatopallidal MSNs, but this effect was not implicated in H3 phosphorylation. The levels of mitogen- and stress-activated kinase 1 (MSK1), which has been reported to mediate ERK-induced H3 phosphorylation, were lower in striatopallidal than in striatonigral MSNs. Moreover, haloperidol-induced H3 phosphorylation was unaltered in MSK1-knockout mice. These data indicate that, in striatopallidal MSNs, H3 phosphorylation is controlled by the opposing actions of D2Rs and A2ARs. Thus, blockade of D2Rs promotes histone H3 phosphorylation via A2AR-mediated activation of Gαolf and inhibition of protein phosphatase-1 via PKA-dependent phosphorylation of DARPP-32.
Related Links	http://dx.doi.org/10.1038/npp.2008.228
Ending Page	1720
Page Count	11
Starting Page	1710
File Format	PDF
ISSN	0893133X
e-ISSN	1740634X
Journal	Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
Issue Number	7
Volume Number	34
Language	English
Publisher Date	2009-06-01
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology Psychiatry and Mental Health

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