Skip to main content
. Author manuscript; available in PMC: 2011 Mar 1.
Published in final edited form as: J Neurosci. 2010 Sep 1;30(35):11565–11575. doi: 10.1523/JNEUROSCI.1746-10.2010

Figure 1. GI-LTP structural plasticity requires NMDARs and CaMKK.

Figure 1

A, Representative fluorescence images of secondary hippocampal dendritic spines visualized using mRFP-βactin for conditions indicated. For some experiments neurons were pretreated with either APV (50 μM, 30 min) or STO-609 (10 μM, 4 hrs) or transfected with plasmid expressing a STO-insensitive mutant of CaMKK (STOins, 24 hrs) prior to GI-LTP treatment (10 min GI-LTP, see Methods). Scale bar is 5 μM. B, Quantitative analysis of spine head width (left panel) and spine length (right panel) for conditions indicated. C, Cumulative distribution plots for spine head width (left panel) and length (right panel) of the population of spines analyzed (n = 75 – 100 spines/neuron; 5 – 6 neurons per coverslip). Error bars indicate SEM (n = 8 – 10 coverslips per condition from 2 – 3 independent cultures). *p<0.05 by Student's t-test.