Increasing evidence supports an important role for the brain's reward circuitry in controlling mood under normal conditions and contributing importantly to the pathophysiology and symptomatology of a range of mood disorders, such as depression. Here we focus on the nucleus accumbens (NAc), a critical component of the brain's reward circuitry, in depression and other stress-related disorders. The prominence of anhedonia, reduced motivation, and decreased energy level in most individuals with depression supports the involvement of the NAc in these conditions. We concentrate on several transcription factors (CREB, ΔFosB, SRF, NFκB, and β-catenin), which are altered in the NAc in rodent depression models-and in some cases in the NAc of depressed humans, and which produce robust depression- or antidepressant-like effects when manipulated in the NAc in animal models. These studies of the NAc have established novel approaches toward modeling key symptoms of depression in animals and could enable the development of antidepressant medications with fundamentally new mechanisms of action.

Original languageEnglish
Title of host publicationNicotine Use in Mental Illness and Neurological Disorders, 2015
EditorsMariella De Biasi
PublisherAcademic Press Inc.
Number of pages20
ISBN (Print)9780128015834
StatePublished - 2015

Publication series

NameInternational Review of Neurobiology
ISSN (Print)0074-7742


  • BDNF
  • CREB
  • Chromatin
  • Dynorphin
  • Epigenetics
  • NFκB
  • Nucleus accumbens
  • Ventral tegmental area
  • ΔFosB
  • β-Catenin


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