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. Author manuscript; available in PMC: 2014 Aug 1.
Published in final edited form as: Biochim Biophys Acta. 2013 Mar 29;1833(8):1820–1831. doi: 10.1016/j.bbamcr.2013.03.021

Figure 4. Activation of cGKII by cGMP causes an increase of cellular surface GluA1.

Figure 4

(A) Cerebellar granule cells maintained for 8 DIV were subjected to different treatments as shown: incubation with 8Br-cGMP (500 μM) for 20 minutes or inhibition with KT5823 during 30 minutes followed by incubation with a GluA1-NT antibody (20 μg/ml) for 20 minutes as indicated in the Methods section. Images represent the immunostaining for synapsin I and GluA1, the merged image and an amplification of each condition. (B) Density of GluA1 clusters in dendrites (clusters/μm). ROI’s of the specific antibody were selected for each condition from at least 15 fields from 2 different experiments. (C) Analysis of the fraction of GluA1 clusters apposed to synapsin I puncta, either upon stimulation or inhibition (n=30 fields from 2 independent experiments). (D) Cumulative probability plots for GluA1 mean fluorescence intensity (mean values: control 19.4±0.06; 8Br-cGMP 23.1±0.11; KT5823 16.4±0.03; 8Br-cGMP+KT 16.7±0.06, a.u.). In B and C the data are represented as the mean ± SEM and analyzed with an unpaired, two-sample t test (*p<0.001). The Komolgorov-Smirnov test was used for the cumulative probability. Scale bars: 10 μm.