Fig. 6.

NMDA receptor- and Ca²⁺-dependent signaling pathways are required for D₂-like antagonist-induced striatal H3 phospho-acetylation. (a) Immunoblots showing levels of H3pS10-acK14 and H4acK12 in striatum of rats treated first with saline or the NMDA receptor antagonist MK-801, followed after 15 min by a single dose of haloperidol or saline. Animals were sacrificed 30 min after the second injection. Notice that pre-treatment with MK-801 blocks the haloper-idol-induced increase in H3pS10-acK14. (b, c) Bar graphs summarizing levels of H3pS10-acK14 (mean ± S.E.M.) in (b) mice and (c) rats treated first with MK801 or saline followed by haloperidol or saline. (d) Representative immunoblots of primary striatal cultures treated with vehicle or glutamate for 30 min, with or without pre-treatment with MK-801 for 30 minutes. Notice that glutamate treatment increases levels of H3pS10-acK14, and notice that this effect is blocked by MK801. (e) Representative immunoblot of dissociated striatal culture treated with vehicle or the l-type Ca²⁺ channel agonist FPL 64176. (f) Levels of H3pS10-acK14 immunoreactivity in striatal cultures after treatment with vehicle, glutamate (±pre-treatment with MK-801) and FPL 64176. Notice that glutamate treatment upregulates H3pS10-acK14, and this is blocked by pre-treatment with MK-801. Notice further that the l-type Ca²⁺ channel agonist FPL 64176 upregulates H3pS10-acK14.