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. 2004 Jun 9;24(23):5283–5291. doi: 10.1523/JNEUROSCI.1224-04.2004

Figure 2.

Figure 2.

Distinct effects of DA receptor antagonists on αCaMKII autophosphorylation and corticostriatal LTP formation. A, Western blot analysis of total αCaMKII (bottom) and p286-αCaMKII (top) in TIFs obtained from control, 3 μm l-sulpiride-treated, or 10 μm SCH 23390-treated corticostriatal slices; the same amount of protein was loaded per lane (p < 0.01, l-sulpiride vs control; p < 0.05, SCH 23390 vs control). *p < 0.01, l-sulpiride versus control; **p < 0.05, SCH 23390 versus control. B, TIF proteins from treated corticostriatal slices were immunoprecipitated with an NR2A-NR2B polyclonal antibody. Western blot analysis was performed in the immunoprecipitated (i.p.) material with αCaMKII and NR2A-NR2B antibodies (+73.4 ± 17.5%, p < 0.05, SCH 23390 vs control; -79.5 ± 10.2%, p < 0.01, l-sulpiride vs control). C, Changes in corticostriatal EPSP amplitude after tetanic stimulation under control conditions, in the presence of 3 μm l-sulpiride-treated slices (p < 0.05; control vs l-sulpiride measured 30 min after the induction; n = 23), in 10 μm SCH 23390-treated slices (p < 0.001; control vs SCH 23390 measured 30 min after the induction; n = 20), and after in vivo intrastriatal administration of 3 mm SCH 23390 (p < 0.001; control vs SCH 23390 intrastriatally at 30 min after induction; n = 13). D, Limb-use asymmetry induced in control rats 24 hr after the injection of 3 mm SCH 23390 (**p < 0.001; SCH 23390 intrastriatally vs sham; n = 8) ipsi, Ipsilateral; contra, contralateral. E, Western blot analysis of active p286-αCaMKII and total αCaMKII in TIFs obtained from treated corticostriatal slices. F, TIF proteins from treated corticostriatal slices were immunoprecipitated with an NR2A-NR2B polyclonal antibody. Western blot analysis was performed in the immunoprecipitated material with αCaMKII and NR2A-NR2B antibodies. WB, Western blot. L-sul, l-sulpiride; SCH, SCH 23390; i.s., intrastriatal; Forsk, forskolin.