The Journal of Neuroscience, February 1, 2006, ():
Cocaine Increases Actin Cycling: Effects in the Reinstatement Model of Drug Seeking
J. Neurosci. Toda et al.
26: 1579
Supplemental data
Files in this Data Supplement:
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Figure Legend. Postulated model of how changes in ABPs increase F-actin by increasing actin cycling after repeated cocaine and decreasing actin depolymerization after acute cocaine. Control (Sa/Sa): The relative balance of ABPs regulating actin cycling and polymerization as filopodia and lamellipodia under control conditions. Acute Cocaine (Sa/Coc): increases p-cofilin which reduces depolymerization and nucleation of F-actin. Reduced capping of the barbed end by phosphorylating adducin promotes polymerization (presumably more as filopodia-like protein complexes due to decreased nucleation by cofilin). Repeated Cocaine (Coc/Sa): increases both depolymerization and polymerization (i.e. increased actin cycling). Decreased LIMK reduces p-cofilin formation to promote depolymerization and nucleation. Elevated p-cortactin and Ena/Vasp reduces formation of lamellipodia-like protein complexes at sites of nucleation, while elevated Ena/Vasp and p-Vasp promote uncapping of the barbed end and filopodia formation. Changes in protein content and phosphorylation are indicated by the size of arrows, symbols and letters. Large arrows to left of Sa/Coc and Coc/Sa indicate the relative direction of change in F-actin.
