Skip to main content
. 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 7.

Figure 7

Haloperidol-induced histone H3 phosphorylation in striatopallidal MSNs is independent of MSK1. Wild type (WT) or MSK1 knock out (KO) mice were treated with vehicle or haloperidol and perfused 15 min later. (a) Phospho-Ser10-acetyl-Lys14-histone H3 (P-AcH3) immunoreactivity in single confocal sections of the dorsomedial (DM) or dorsolateral (DL) striata of WT and MSK1 KO mice. (b, c) Quantification of (b) diphospho-Thr202/Tyr204-ERK1/2 (P-ERK) and (c) P-AcH3 immunoreactive neurons in the DM (b, c) and DL (c) striata of WT and MSK1 KO mice 15 min after administration of vehicle (Veh) or haloperidol (Hal). No difference in P-AcH3 immunoreactivity was found between vehicle treated WT mice and vehicle treated MSK1 KO mice (the latter are not shown in the figure) (*** p < 0.001 vs. Veh WT). (d) Double immunofluorescence showing P-ERK (green) and P-AcH3 (red) in the DM of WT and MSK1 KO mice after haloperidol treatment. Arrowheads indicate colocalization of P-ERK and P-AcH3 immunoreactivity in the same MSNs. Scale bars: 40 µm.

HHS Vulnerability Disclosure