Skip to main content
. 2014 Feb 5;34(6):2051–2064. doi: 10.1523/JNEUROSCI.2795-13.2014

Figure 4.

Figure 4.

The nicotine effect on GluA1-SEP FRAP is restricted to spines and represents a change in the rate of exchange between spine and dendrite surface receptors. A, Representative images depicting the bleaching of a spine-sized area of GluA1-SEP on the dendrite. The bleached region and region measured for FRAP were the same, represented by the outlined area. Scale bar, 2 μm. B, FRAP is quite rapid on the dendrite, and there is no difference in mobility of GluA1-SEP on the dendrite between control and nicotine-treated cells (Ctrl vs Nic: 102 ± 3 vs 101 ± 2%; n = 14,15; p = 0.87). C, Representative images depicting bleach of GluA1-SEP signal along 10 μm of the dendrite surrounding a bleached spine. Solid outline indicates the region used to measure FRAP. Dotted outline represents the entire area that was bleached. Scale bar, 3 μm. D, When the reserve pool of surface fluorescent receptors is depleted, GluA1-SEP recovery at the spine is greatly attenuated both in control and nicotine-treated cells, indicating that previously observed recoveries represented exchange between receptor pools on spines and dendrites (Ctrl vs Nic: 55 ± 3 vs 50 ± 3%; n = 12,12; p = 0.28).