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. 2010 Nov 8;107(47):20559–20564. doi: 10.1073/pnas.1010346107

Fig. 5.

Fig. 5.

Stimuli that target CaMKIIα to inhibitory synapses increase surface GABAAR expression. (A) Neurons treated with NMDA or glutamate for 1 min were labeled for surface-expressed GABAAR β2/3 subunits. (Scale bar, 10 μm.) (B) Changes in surface receptor labeling intensity are shown as a percentage of untreated control levels. *P < 0.05; **P < 0.01; ***P < 0.001. (C) Neurons transfected with WT or mutant mGFP-CaMKIIα were treated with NMDA and labeled for surface GABAAR β2/3 subunits. Representative images show dendritic mGFP-CaMKIIα and GABAAR staining. (D and E) Quantification of dendritic GABAAR β2/3 surface staining of WT and mutant mGFP-CaMKIIα–transfected neurons. Changes in fluorescence values are presented as the percent of WT control neurons. *P < 0.05; **P < 0.01. (F) NMDA induced a significant decrease in surface GABAAR levels in K42M- and W237K-transfected neurons that is blocked by the CaN inhibitor CSA. Representative dendrites show surface GABAAR labeling. (Scale bar, 10 μm.) (G) Surface GABAAR expression is presented as the percent of control levels for each mutant. *P < 0.05; **P < 0.01.