The Brain Reward Circuitry in Mood Disorders

By S. Russo, E. Nestler. Nature Reviews Neuroscience, 2013

1,712 citations recorded by the source corpus.

Mood disorders are common and debilitating conditions characterized in part by profound deficits in reward-related behavioural domains. A recent literature has identified important structural and functional alterations within the brain's reward circuitry — particularly in the ventral tegmental area–nucleus accumbens pathway — that are associated with symptoms such as anhedonia and aberrant reward-associated perception and memory. This Review synthesizes recent data from human and rodent studies from which emerges a circuit-level framework for understanding reward deficits in depression. We also discuss some of the molecular and cellular underpinnings of this framework, ranging from adaptations in glutamatergic synapses and neurotrophic factors to transcriptional and epigenetic mechanisms.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/811a54711ccacda19526f41498d59c101afc944b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. G. Sanacora
2. R. Duman
3. John H. Krystal
4. P. Belujon
5. Anthony A. Grace
6. Lucy K. Bicks
7. Aleksandra Kupferberg
8. G. Hasler

In Molecular Biology

1. Anthony A. Grace
2. Lucy K. Bicks
3. R. Duman
4. Aleksandra Kupferberg
5. P. Belujon
6. G. Hasler
7. E. Nestler

Citations in the corpus

• Pathophysiology of Migraine: A Disorder of Sensory Processing. (2017, background): “The VTA is also involved in nociceptive processing (34, 64, 230, 698), food reward, drug addiction (479, 600), and mood disorders (697).”
• Social functioning in major depressive disorder. (2016, positive): “…mice show distinct cellular and circuit alterations between the NAcc and other brain regions within the reward circuitry, demonstrating a causal role for plasticity in this circuit in mediating social anhedonia in a mouse model of depression (Heshmati and Russo, 2015; Russo and Nestler, 2013).”
• Altered connectivity in depression: GABA and glutamate neurotransmitter deficits and reversal by novel treatments (2019, background): “There is also evidence that social defeat and chronic stress increase mesolimbic dopamine system activity and that these changes are associated with reduction in social interaction and depressive behaviors (Russo and Nestler, 2013).”
• Psychedelics Promote Structural and Functional Neural Plasticity (2018, background): “Depression, post-traumatic stress disorder (PTSD), and addiction share common neural circuitry (Arnsten, 2009; Russo et al., 2009; Peters et al., 2010; Russo and Nestler, 2013) and have high comorbidity (Kelly and Daley, 2013).”
• Dopamine System Dysregulation in Major Depressive Disorders (2017, background): “The VTA receives GABAergic projections from the rostromedial tegmentum as well as the VP and glutamatergic projections from the lateral habenula, among others (Russo and Nestler, 2013).”