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. Author manuscript; available in PMC: 2009 Oct 7.
Published in final edited form as: Neuropsychopharmacology. 2009 Jan 21;34(7):1710–1720. doi: 10.1038/npp.2008.228

Figure 1.

Figure 1

Effect of haloperidol on histone H3 phosphorylation and acetylation in striatal MSNs. Mice expressing EGFP in striatonigral (Drd1a-EGFP) or striatopallidal (Drd2-EGFP) MSNs were treated with vehicle or haloperidol and perfused 15 min (15’; a–f), or 60 min later (60’; b, d). (a, c, e). Confocal sections of the dorsal striatum, showing immunofluorescence (red) for phospho-Ser10-histone H3 (P-H3, a), phospho-Ser10-acetyl-Lys14-histone H3 (P-AcH3, c) and acetyl-Lys14-histone H3 (AcH3, e) alone (left panels), or in combination with EGFP fluorescence (green; right panels). (b, d, f) Quantification of P-H3- (b), P-AcH3- (d), andAcH3- (f) immunoreactive neurons among EGFP-positive (EGFP+) or EGFP-negative (EGFP-) neurons in the dorsomedial (DM) and dorsolateral (DL) striata of vehicle (Veh) or haloperidol (Hal) treated Drd2-EGFP mice (*** p < 0.001 vs. Veh; °°°p < 0.001 vs. Hal 15’). Scale bars: 40 µm.

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