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. Author manuscript; available in PMC: 2010 May 25.
Published in final edited form as: J Neurosci. 2009 Nov 25;29(47):14903–14911. doi: 10.1523/JNEUROSCI.3436-09.2009

Figure 2. PKA mediates D1R-dependent dephosphorylation of Cx36 at Ser293 in AII amacrine cells.

Figure 2

A & B, Under control conditions Ser293-P (green) labeling of Cx36 gap junctions (mCx36, red) on AII amacrine cells (calretinin, blue) was heterogeneous. Annotated arrowheads indicate pairs of Cx36 plaques along single dendrites that are in different phosphorylation states. The close proximity of Cx36 plaques with widely varying Ser293-P labeling implies that regulation is locally controlled at individual plaques. C & D, D1R activation (SKF38393, 100 µM) greatly diminished Ser293-P labeling. E & F, Inhibition of PKA (Rp-8-CPT-cAMPS, 20 µM) attenuated the dramatic reduction in Ser293-P labeling caused by SKF38393 (100 µM). G & H, Antagonism of D1Rs (SCH23390, 100 µM) increased Ser293-P labeling. I, Summary of data shows that inhibition of PKA significantly suppressed the reduction in Ser293 phosphorylation caused by D1R activation. J, Summary of data shows that changes in the percentage of Cx36 plaques that show detectable Ser293-P labeling follows the same pattern established for relative Ser293-P measurements in I. Error bars are s.e.m, n = 6. Asterisk denotes P < 0.05, two asterisks denote P < 0.01. Images are 1 µm-deep stacks. Scale bar in H is 10 µm.