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. Author manuscript; available in PMC: 2014 Oct 20.
Published in final edited form as: J Neurochem. 2004 Sep;90(5):1117–1131. doi: 10.1111/j.1471-4159.2004.02569.x

Fig. 4.

Fig. 4

Blockade of D2-like signaling induces H3 phospho-acetylation in striatum with kinetics that are characteristic of the early response. (a) Representative immunoblots from striatum of haloperidol-treated mice at 15, 30 and 480 min after a single dose (1mg/kg), and after regular treatments twice daily (1mg/kg) for a period of 10 days. Notice increased levels of H3pS10-acK14 in striatum at 15 and 30 min after acute haloperidol treatment. (b) Kinetics of H3 phospho-acetylation in striatum of haloperidol-treated mice. Data are normalized to levels of saline-treated controls and expressed as mean ± S.E.M. (*p < 0.05, anova with Fisher's paired least significant difference (PLSD) corrected for multiple comparisons). There is a significant increase in striatal H3pS10-acK14 at 15, 30 and 120 min after a single dose, and return to baseline levels at 480 min. Notice normal levels of phospho-acetylated H3 in striatum of animals subject to repeated haloperidol treatment for 1, 3, 5 or 10 days. Animals that were subject to repeated treatments were killed 120 min after the last treatment.