Activin receptor signaling regulates cocaine-primed behavioral and morphological plasticity

Nat Neurosci. 2015 Jul;18(7):959-61. doi: 10.1038/nn.4036. Epub 2015 Jun 1.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Activin Receptors / metabolism*
  • Animals
  • Behavior, Animal / drug effects*
  • Cocaine / administration & dosage
  • Cocaine / pharmacology*
  • Dendritic Spines / drug effects
  • Dopamine Uptake Inhibitors / administration & dosage
  • Dopamine Uptake Inhibitors / pharmacology*
  • Male
  • Neuronal Plasticity / drug effects*
  • Nucleus Accumbens / cytology
  • Nucleus Accumbens / drug effects*
  • Rats
  • Rats, Sprague-Dawley
  • Self Administration
  • Signal Transduction / drug effects*
  • Signal Transduction / genetics
  • Smad3 Protein / metabolism*

Substances

  • Dopamine Uptake Inhibitors
  • Smad3 Protein
  • Smad3 protein, rat
  • Activin Receptors
  • Cocaine