Figure 5.

Histone H3 phosphorylation induced by blockade of D2Rs is independent of ERK activation. (a) Mice expressing EGFP in striatonigral (Drd1a-EGFP) or striatopallidal (Drd2-EGFP) MSNs were treated with vehicle, haloperidol, or raclopride, and perfused 15 min later. EGFP fluorescence (green) in single confocal sections of the dorsomedial (DM) or dorsolateral (DL) striatum is shown in combination with fluorescence (red) for diphospho-Thr202/Tyr204-ERK1/2 (P-ERK). Note, in haloperidol and raclopride treated mice, the relatively low number and prevalent localization in the DM of P-ERK-positive MSNs (single-labeled Drd1a-EGFP mice and double-labeled in Drd2-EGFP mice). (b–e) Wild type mice were treated with haloperidol alone or in combination with the MEK inhibitor SL327 (injected 45 min prior to haloperidol) and perfused 15 min later. P-ERK (b, d) and phospho-Ser10-acetyl-Lys14-histone H3 (P-AcH3) (c, e) immunoreactivity was determined in single confocal sections of the DM striatum. (d, e) Quantification of striatal P-ERK (d) and P-AcH3 (e) immunoreactive neurons in the DM and DL striata of mice treated with vehicle (Veh) or haloperidol (Hal) alone or in combination with SL327 (* p < 0.05 vs. vehicle; °p < 0.05 vs. Hal). Scale bars: 40 µm.