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Activin receptor signaling regulates cocaine-primed behavioral and morphological plasticity.

Nature neuroscience (2015-06-02)
Amy M Gancarz, Zi-Jun Wang, Gabrielle L Schroeder, Diane Damez-Werno, Kevin M Braunscheidel, Lauren E Mueller, Monica S Humby, Aaron Caccamise, Jennifer A Martin, Karen C Dietz, Rachael L Neve, David M Dietz
ABSTRAKT

Activin receptor signaling, including the transcription factor Smad3, was upregulated in the rat nucleus accumbens (NAc) shell following withdrawal from cocaine. Direct genetic and pharmacological manipulations of this pathway bidirectionally altered cocaine seeking while governing morphological plasticity in NAc neurons. Thus, Activin/Smad3 signaling is induced following withdrawal from cocaine, and such regulation may be a key molecular mechanism underlying behavioral and cellular plasticity in the brain following cocaine self-administration.

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Sigma-Aldrich
PhosphoDetect Anti-Smad3 (pSer423/425) królicze mAb (C25A9), liquid, clone C25A9, Calbiochem®