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. Author manuscript; available in PMC: 2010 Feb 12.
Published in final edited form as: Neuron. 2009 Feb 12;61(3):425–438. doi: 10.1016/j.neuron.2008.12.015

Figure 5. Association of CaMKIIα with D3Rs in accumbal neurons in vivo.

Figure 5

(A and B) Coimmunoprecipitation (IP) of CaMKIIα and D3Rs in the synaptosomal fraction from the rat NAc. Lanes 3 and 4 showed no specific bands due to the lack of any antibody (L3) and the use of an irrelevant IgG (L4). (C and D) No coimmunoprecipitation of CaMKIIα and D3Rs was detected in the synaptosomal fraction from the rat substantia nigra (SN)/ventral tegmental area (VTA) and medial mammillary bodies (MMB). (E) Ionomycin (15 min) concentration-dependently increased the association of CaMKIIα and pCaMKIIα (T286) with D3Rs. (F) KN93 blocked the effect of ionomycin. Ionomycin (10 μM) was co-treated with KN93 or KN92 (20 μM) for 15 min. (G) Tat-CaMKIINtide blocked the effect of ionomycin. Tat-CaMKIINtide (5 μM) was applied 1 h prior to ionomycin (10 μM, 15 min). (H) Tat-D3Rr blocked the ionomycin-induced association of CaMKIIα with D3Rs. (I) Tat-D3Rr blocked the ionomycin-stimulated serine phosphorylation of D3Rs. Tat peptides (5-10 μM) were applied 1 h prior to ionomycin (10 μM, 15 min). Immunoblots (IB) of CaMKIIα, pCaMKIIα (T286), phosphoserine, or D3Rs were performed on D3R precipitates from drug-treated accumbal slices (E–G). Data are presented as means ± SEM for 3–5 experiments per group. *p < 0.05 versus vehicle or vehicle + vehicle. +p < 0.05 versus vehicle + ionomycin.