Homeostatic plasticity during alcohol exposure promotes enlargement of dendritic spines

Abstract

In the published paper of Carpenter-Hyland & Chandler (2006), there was an error in Fig. 3A. Panel 3A should have been labeled F-Actin (not PSD-95). We apologize for this error, and reproduce the corrected Fig. 3 on the next page with its legend. The size of dendritic clusters of F-actin increase in response to chronic d(–)-2-amino-5-phosphono-pentanoic acid (APV) or ethanol exposure. (A–C) Staining of F-actin with Alexa 594-conjugated phalloidin was used to examine alterations in dendritic spines induced by prolonged exposure to APV (4 days, 100 µm) and ethanol (4 days, 50 mm) (A). Cluster analysis revealed that APV increased F-actin cluster size (B) and density (C) in virtually all neurons in the culture dish. Scale bar: 20 µm. (D–G) Similar to APV, chronic ethanol increased dendritic F-actin clusters. (D) Representative images of dendritic F-actin clusters. Scale bar: 5 µm. (E) Following prolonged ethanol exposure, the number of neurons in the culture dish with F-actin clusters that averaged at least a twofold increase in size was dependent upon the ethanol concentration. N-methyl-d-aspartate (NMDA; 2.5 µm; N, NMDA) reversed the effect of ethanol (50 mm). Cluster analysis revealed that ethanol greatly enhanced F-actin cluster size (F), with smaller increases in cluster density (G). NMDA alone slightly reduced F-actin cluster size and density, but completely blocked the ethanol-induced increases (F and G). (B and C) *Significant difference from control (P < 0.01). Student's t-test, n = 20. (E) *P < 0.05; **P < 0.01, compared with control; #P < 0.01, compared with ethanol. anova with SNK, n = 6. (F and G) *P < 0.05; **P < 0.01, compared with control; #P < 0.05; ##P < 0.01, compared with ethanol. anova with SNK, n = 20. A, APV; C, Control; E, EtOH; N, NMDA.