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. 1998 Dec 1;18(23):9835–9844. doi: 10.1523/JNEUROSCI.18-23-09835.1998

Fig. 6.

Fig. 6.

Prevention of NMDA-induced spine loss by jasplakinolide. A, B, F-actin labeling in cultures treated with 50 μm NMDA after preincubation in the absence (A) or presence (B) of the actin-stabilizing compound jasplakinolide (2 μm; 2 hr). This compound competes with phalloidin for binding to F-actin. To obtain similar pixel intensities, we collected the image in B using a fivefold longer shutter open time than that used to collect the image inA. This 80% decrease in phalloidin-staining intensity confirms the presence of jasplakinolide bound to intracellular actin filaments. C, Quantification of the protective effect of jasplakinolide (Jasp) on NMDA-induced loss of F-actin punctae (spines). Vertical bars indicate means; error bars indicate SEM (n = 10). NMDA caused a statistically significant loss of F-actin punctae that was fully prevented by preincubation with Jasp (2 μm; 2 hr). The density of F-actin punctae was significantly different in all three experimental groups compared with control (p < 0.05, Dunnett’s post hoc test). D–F. Dendritic spines preserved in the presence of NMDA, in parallel with the preservation of F-actin punctae. DiI-labeled neurons from cultures treated with 50 μm NMDA after preincubation in the absence (D) or presence (E) of jasplakinolide (2 μm; 2 hr), illustrating that the drug indeed prevents spine loss in addition to F-actin loss.F, Enlargement of boxed region inE.