Drugs of abuse, including alcohol, can promote maladaptive synaptic plasticity mechanisms in the brains reward system, but the underlying molecular pathways are not well characterized. Now, Ron and colleagues highlight a key role of the serine/threonine kinase complex mammalian target of rapamycin complex 1 (mTORCl) in the nucleus accumbens (NAc) in mediating synaptic changes that accompany alcohol addiction.
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