The DOI matches its Crossref record; 210 of the 210 references it cites were found in a registry or an index; 1 of the 217 sources its claims cite were checked for support.
The molecular and cellular mechanisms of depression: a focus on reward circuitry
Open accessAbstract
Depression is a complex disorder that takes an enormous toll on individual health. As affected individuals display a wide variation in their clinical symptoms, the precise neural mechanisms underlying the development of depression remain elusive. Although it is impossible to phenocopy every symptom of human depression in rodents, the preclinical field has had great success in modeling some of the core affective and neurovegetative depressive symptoms, including social withdrawal, anhedonia, and weight loss. Adaptations in select cell populations may underlie these individual depressive symptoms and new tools have expanded our ability to monitor and manipulate specific cell types. This review outlines some of the most recent preclinical discoveries on the molecular and neurophysiological mechanisms in reward circuitry that underlie the expression of behavioral constructs relevant to depressive symptoms.
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TL;DR
This review synthesizes preclinical evidence on molecular and cellular adaptations in ventral tegmental area (VTA) and nucleus accumbens (NAc) reward circuitry that underlie depression-like behaviors, especially anhedonia and social withdrawal. It emphasizes cell-type-specific and sometimes bidirectional changes across stress models and calls for more work on non-neuronal cells, sex differences, and treatment-resistant depression.
Key findings
- Stress produces divergent VTA dopamine neuron activity: chronic social defeat stress (CSDS) increases VTA dopamine neuron firing, with increased Ih currents in NAc-projecting but not mPFC-projecting neurons; inhibiting NAc-projecting VTA dopamine neurons induces resilience, whereas inhibiting mPFC projections promotes susceptibility. Chronic mild or cold stress instead reduces VTA population activity, an effect more pronounced in females.
- In NAc, chronic stress causes opposing medium spiny neuron (MSN) subtype changes: excitatory input is weakened onto D1-MSNs and strengthened onto D2-MSNs; optogenetic D1-MSN stimulation reverses social and sucrose preference deficits, while D2-MSN stimulation enhances stress susceptibility. D1-MSN dendritic complexity is reduced in CSDS-susceptible mice, and D1-MSN RhoA/Egr3 signaling promotes susceptibility.
- Molecular adaptations include BDNF-TrkB, AKT, ERK2, Cdk5, Otx2, CREB/ΔFosB, β-catenin/Dicer1, Dnmt3a, Tet1, H3.3, and SIRT1, with cell-type-specific examples such as decreased Slc6a15 in D2-MSNs and decreased Nlgn2 in D1-MSNs of susceptible mice.
- Non-neuronal and neuroimmune mechanisms are implicated: at least 40% of cells in rodent and human brain are non-neuronal; chronic stress increases IL-6, IL-1β, and CXCL1, recruits monocytes/macrophages, and alters microglia, while anti-inflammatory treatments reduce depressive symptoms in humans. Approximately 95% of NAc neurons are MSNs, but cholinergic interneurons and glia also contribute.
Methods
- Design: narrative review of preclinical rodent models for depression-like behavior—chronic unpredictable stress (CUS; 8–12 weeks), learned helplessness, and CSDS (10 days; approximately 70% stress-susceptible, ~30% stress-resilient)—integrated with human functional imaging and postmortem MDD findings.
- Data or sample: no new experimental data; synthesizes cited rodent studies using male, female, and adolescent mice/rats, plus human postmortem MDD tissue and imaging studies.
- Main analysis: qualitative synthesis of electrophysiological, optogenetic, viral, transcriptomic, epigenetic, structural, and behavioral findings, with proposed remaining questions rather than a systematic or quantitative meta-analysis.
Limitations
- The paper states that many questions remain, including whether bidirectional VTA activity changes reflect stress paradigm, symptom type, or distinct cell populations; most NAc D1/D2-MSN work was done solely in male rodents; validation relies heavily on postmortem MDD tissue often from suicide completers; and new antidepressants have not been approved despite rodent progress.
- The paper states that preclinical models cannot phenocopy all human depression symptoms, that forced-swim/tail-suspension interpretations have been questioned, and that treatment-resistant populations are understudied.
- Evident from the text: as a narrative review, it lacks a systematic search or meta-analysis, and conclusions depend on cited studies with heterogeneous stress paradigms, housing conditions, sex inclusion, and cell-type specificity.
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Claims the paper makes
160 Not checked yet · 7 Own interpretation · 1 Supported so far
In the paper
“The remaining ~30% of mice retain preference for social interaction and are termed “stress-resilient.””
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Social defeat stress
What the sources say
- Not checked yetcites [13] Krishnan V, Han M-HH, Graham DL, Berton O, Renthal W, Russo SJ, et al. Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions. Cell. 2007;131:391–404. source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Chronic physical or psychosocial stressors increase VTA dopamine neuron activity to elicit depression-like behavior.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [13] Krishnan V, Han M-HH, Graham DL, Berton O, Renthal W, Russo SJ, et al. Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions. Cell. 2007;131:391–404. source
- Not checked yetcites [23] Chaudhury D, Walsh JJ, Friedman AK, Juarez B, Ku SM, Koo JW, et al. Rapid regulation of depression-related behaviours by control of midbrain dopamine neurons. Nature. 2013;493:532–6. source
- Not checked yetcites [24] Wook Koo J, Labonté B, Engmann O, Calipari ES, Juarez B, Lorsch Z, et al. Essential role of mesolimbic brain-derived neurotrophic factor in chronic social stress–induced depressive behaviors. Biol Psychiatry. 2016;80:469–78. source
- Not checked yetcites [25] Friedman AK, Juarez B, Ku SM, Zhang H, Calizo RC, Walsh JJ, et al. KCNQ channel openers reverse depressive symptoms via an active resilience mechanism. Nat Commun. 2016;7:11671. source
- Not checked yetcites [26] Isingrini E, Perret L, Rainer Q, Amilhon B, Guma E, Tanti A, et al. Resilience to chronic stress is mediated by noradrenergic regulation of dopamine neurons. Nat Neurosci. 2016;19:560–3. source
- Not checked yetcites [27] Li L, Sun H, Ding J, Niu C, Su M, Zhang L, et al. Selective targeting of M-type potassium Kv 7.4 channels demonstrates their key role in the regulation of dopaminergic neuronal excitability and depression-like behaviour. Br J Pharmacol. 2017;174:4277–94. source
- Not checked yetcites [28] Razzoli M, Andreoli M, Michielin F, Quarta D, Sokal DM. Increased phasic activity of VTA dopamine neurons in mice 3 weeks after repeated social defeat. Behav Brain Res. 2011;218:253–7. source
- Not checked yetcites [29] Cao J-LJ-L, Covington HE, Friedman AK, Wilkinson MB, Walsh JJ, Cooper DC, et al. Mesolimbic dopamine neurons in the brain reward circuit mediate susceptibility to social defeat and antidepressant action. J Neurosci. 2010;30:16453–8. source
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In the paper
“Compounds that produce acute behavioral effects in a forced-swim or tail-suspension test (i.e., increase struggling time) may not translate to meaningful therapeutics when administered chronically”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction
What the sources say
- Not checked yetcites [9] Anyan J, Amir S. Too depressed to swim or too afraid to stop? A reinterpretation of the forced swim test as a measure of anxiety-like behavior. Neuropsychopharmacology. 2018;43:931–3. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Stressed animals also tend to spend less time struggling against inescapable stressors such as forced swimming or tail suspension.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction
What the sources say
- Not checked yetcites [7] Czéh B, Fuchs E, Wiborg O, Simon M. Animal models of major depression and their clinical implications. Prog Neuropsychopharmacol Biol Psychiatry. 2016;64:293–310. source
- Not checked yetcites [8] Nestler EJ, Hyman SE. Animal models of neuropsychiatric disorders. Nat Neurosci. 2010;13:1161–9. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“they also respond to aversive events [21, 22]”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [21] Matsumoto M, Hikosaka O. Two types of dopamine neuron distinctly convey positive and negative motivational signals. Nature. 2009;459:837–41. source
- Not checked yetcites [22] Cohen JY, Haesler S, Vong L, Lowell BB, Uchida N. Neuron-type-specific signals for reward and punishment in the ventral tegmental area. Nature. 2012;482:85–8. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Chronically stressed rodents have reduced reward preference, as measured by a loss of preference for sucrose solutions and time spent interacting with a novel con-specific.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction
What the sources say
- Not checked yetcites [7] Czéh B, Fuchs E, Wiborg O, Simon M. Animal models of major depression and their clinical implications. Prog Neuropsychopharmacol Biol Psychiatry. 2016;64:293–310. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“human functional imaging and postmortem tissue studies have identified abnormalities in several brain regions [2–6] including nuclei within the brain’s reward pathway.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction
What the sources say
- Not checked yetcites [2] Drevets WC. Neuroimaging and neuropathological studies of depression: implications for the cognitive-emotional features of mood disorders. Curr Opin Neurobiol. 2001;11:240–9. source
- Not checked yetcites [3] Liotti M, Mayberg HS. The role of functional neuroimaging in the neuropsychology of depression. J Clin Exp Neuropsychol. 2001;23:121–36. source
- Not checked yetcites [4] Nestler EJ, Barrot M, DiLeone RJ, Eisch AJ, Gold SJ, Monteggia LM. Neurobiology of depression. Neuron. 2002;34:13–25. source
- Not checked yetcites [5] Zhu M-Y, Klimek V, Dilley GE, Haycock JW, Stockmeier C, Overholser JC, et al. Elevated levels of tyrosine hydroxylase in the locus coeruleus in major depression. Biol Psychiatry. 1999;46:1275–86. source
- Not checked yetcites [6] Drysdale AT, Grosenick L, Downar J, Dunlop K, Mansouri F, Meng Y, et al. Resting-state connectivity biomarkers define neurophysiological subtypes of depression. Nat Med. 2017;23:28–38. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“burst firing is increased in vivo during an encounter with an aggressive rat [32].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [32] Anstrom KK, Miczek KA, Budygin EA. Increased phasic dopamine signaling in the mesolimbic pathway during social defeat in rats. Neuroscience. 2009;161:3–12. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The stress-mediated increases in VTA dopamine neuron firing are caused by increased Ih currents [29, 35]”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [29] Cao J-LJ-L, Covington HE, Friedman AK, Wilkinson MB, Walsh JJ, Cooper DC, et al. Mesolimbic dopamine neurons in the brain reward circuit mediate susceptibility to social defeat and antidepressant action. J Neurosci. 2010;30:16453–8. source
- Not checked yetcites [35] Wanat MJ, Hopf FW, Stuber GD, Phillips PEM, Bonci A. Corticotropin-releasing factor increases mouse ventral tegmental area dopamine neuron firing through a protein kinase C-dependent enhancement of I h. J Physiol. 2008;586:2157–70. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Dendritic spine density, a proxy for excitatory synapse density and activity, is also increased in the VTA of CSDS-susceptible mice [33].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [33] Qu Y, Yang C, Ren Q, Ma M, Dong C, Hashimoto K. Regional differences in dendritic spine density confer resilience to chronic social defeat stress. Acta Neuropsychiatr. 2018;30:117–22. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 49
- Probably not a substantial claim. 4
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“CB2 activation reduces VTA dopamine neuron firing [39] and immobility in forced-swim and tail-suspension tests [40].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Supportedcites [39] Zhang H-Y, Gao M, Liu Q-R, Bi G-H, Li X, Yang H-J, et al. Cannabinoid CB2 receptors modulate midbrain dopamine neuronal activity and dopamine-related behavior in mice. Proc Natl Acad Sci USA. 2014;111:E5007–15. source
Citation [39] is attached only to the claim about VTA dopamine neuron firing; the immobility claim is attributed to [40]. In “CB2R Activation Inhibits VTA DA Neuronal Firing” (page not provided), the paper reports that CB2 receptor agonists inhibited VTA dopamine neuronal firing. (LLM, conf=0.94)
- Not checked yetcites [40] Bahi A, Al Mansouri S, Al Memari E, Al Ameri M, Nurulain SM, Ojha S. β-Caryophyllene, a CB2 receptor agonist produces multiple behavioral changes relevant to anxiety and depression in mice. Physiol Behav. 2014;135:119–24. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Supported
In the paper
“The stress-induced behavioral phenotypes are reversed by chronic, but not acute antidepressant treatment, and are thus posited to have both face and predictive validity [8].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction
What the sources say
- Not checked yetcites [8] Nestler EJ, Hyman SE. Animal models of neuropsychiatric disorders. Nat Neurosci. 2010;13:1161–9. source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Reward learning and connectivity between the VTA and striatum is impaired in MDD patients [18, 19].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [18] Kumar P, Goer F, Murray L, Dillon DG, Beltzer ML, Cohen AL, et al. Impaired reward prediction error encoding and striatal-midbrain connectivity in depression. Neuropsychopharmacology. 2018;43:1581–8. source
- Not checked yetcites [19] Blood AJ, Iosifescu DV, Makris N, Perlis RH, Kennedy DN, Dougherty DD, et al. Microstructural abnormalities in subcortical reward circuitry of subjects with major depressive disorder. PLoS ONE. 2010;5:e13945. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“dopaminergic neurons in the VTA fire in response to unpredicted reward and in anticipation of impending reward [20]”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [20] Schultz W. Reward prediction error. Curr Biol. 2017;27:R369–R371. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“rodents are exposed to a series of stressors such as cage tilting and disrupted lights for 8–12 weeks [10], after which animals show reduced sucrose preference.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Chronic unpredictable stress
What the sources say
- Not checked yetcites [10] Willner P. The chronic mild stress (CMS) model of depression: history, evaluation and usage. Neurobiol Stress. 2017;6:78–93. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Approximately 70% of mice that undergo CSDS are termed “stress-susceptible,” displaying a robust depression-like phenotype marked by reduced social interaction, increased anhedonia, and significant body-weight changes [13].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Social defeat stress
What the sources say
- Not checked yetcites [13] Krishnan V, Han M-HH, Graham DL, Berton O, Renthal W, Russo SJ, et al. Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions. Cell. 2007;131:391–404. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“inhibiting VTA dopamine neurons that project to the NAc induces resilience but inhibiting VTA dopamine projections to medial prefrontal cortex (mPFC) promotes CSDS susceptibility [23].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [23] Chaudhury D, Walsh JJ, Friedman AK, Juarez B, Ku SM, Koo JW, et al. Rapid regulation of depression-related behaviours by control of midbrain dopamine neurons. Nature. 2013;493:532–6. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Increased Ih currents occur specifically in NAc, but not mPFC projecting VTA dopamine neurons [30]”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [30] Friedman AK, Walsh JJ, Juarez B, Ku SM, Chaudhury D, Wang J, et al. Enhancing depression mechanisms in midbrain dopamine neurons achieves homeostatic resilience. Science. 2014;344:313–9. https://doi.org/10.1126/science.1249240 . source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Ih and intrinsic excitability are upregulated in CSDS-susceptible mice [30], but somewhat paradoxically, Ih is upregulated to a greater extent in resilient mice.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [30] Friedman AK, Walsh JJ, Juarez B, Ku SM, Chaudhury D, Wang J, et al. Enhancing depression mechanisms in midbrain dopamine neurons achieves homeostatic resilience. Science. 2014;344:313–9. https://doi.org/10.1126/science.1249240 . source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“KCNQ channel Kv7.4 is an attractive target in depression, as this subtype is more selectively expressed in VTA (not substantia nigra) dopamine neurons and Kv7.4 currents are reduced in susceptible mice [27].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [27] Li L, Sun H, Ding J, Niu C, Su M, Zhang L, et al. Selective targeting of M-type potassium Kv 7.4 channels demonstrates their key role in the regulation of dopaminergic neuronal excitability and depression-like behaviour. Br J Pharmacol. 2017;174:4277–94. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“KCNQ overexpression or administration of KCNQ-openers rescues depressive behavior [25, 27] by reducing firing of NAc projecting, but not PFC projecting VTA dopamine neurons [25].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [25] Friedman AK, Juarez B, Ku SM, Zhang H, Calizo RC, Walsh JJ, et al. KCNQ channel openers reverse depressive symptoms via an active resilience mechanism. Nat Commun. 2016;7:11671. source
- Not checked yetcites [27] Li L, Sun H, Ding J, Niu C, Su M, Zhang L, et al. Selective targeting of M-type potassium Kv 7.4 channels demonstrates their key role in the regulation of dopaminergic neuronal excitability and depression-like behaviour. Br J Pharmacol. 2017;174:4277–94. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Ih potentiation with repeated lamotrigine increases K+ currents and decreases neuronal excitability in previously susceptible mice to reverse social and sucrose preference deficits [25].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [25] Friedman AK, Juarez B, Ku SM, Zhang H, Calizo RC, Walsh JJ, et al. KCNQ channel openers reverse depressive symptoms via an active resilience mechanism. Nat Commun. 2016;7:11671. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Sucrose preference deficits, social avoidance, and VTA excitability are reduced by opening Kv7.4 channels with fasudil [27]”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [27] Li L, Sun H, Ding J, Niu C, Su M, Zhang L, et al. Selective targeting of M-type potassium Kv 7.4 channels demonstrates their key role in the regulation of dopaminergic neuronal excitability and depression-like behaviour. Br J Pharmacol. 2017;174:4277–94. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“chronic stress increases extracellular signal-regulated kinase 2 (ERK2) activity in the VTA and inhibiting VTA ERK2 rescues CSDS-susceptibility and reduces forced-swim and tail-suspension immobility by reducing dopamine neuron excitability [47].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [47] Iñiguez SD, Vialou V, Warren BL, Cao J-L, Alcantara LF, Davis LC, et al. Extracellular signal-regulated kinase-2 within the ventral tegmental area regulates responses to stress. J Neurosci. 2010;30:7652–63. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Rats exposed to chronic mild stress have fewer spontaneously active dopamine neurons [52, 53], an effect more pronounced in females [53].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [52] Moreines JL, Owrutsky ZL, Gagnon KG, Grace AA. Divergent effects of acute and repeated quetiapine treatment on dopamine neuron activity in normal vs. chronic mild stress induced hypodopaminergic states. Transl Psychiatry. 2017;7:1275. source
- Not checked yetcites [53] Rincón-Cortés M, Grace AA. Sex-dependent effects of stress on immobility behavior and VTA dopamine neuron activity: modulation by ketamine. Int J Neuropsychopharmacol. 2017;20:823–32. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“VTA firing is also reduced in mice exposed to CUS and optogenetic stimulation in this context reverses, instead of promotes, stress-induced behavioral deficits [54].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [54] Tye KM, Mirzabekov JJ, Warden MR, Ferenczi EA, Tsai H-C, Finkelstein J, et al. Dopamine neurons modulate neural encoding and expression of depression-related behaviour. Nature. 2013;493:537–41. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“long-term activation of PPARα decreases β2-nAChR phosphorylation, increases dopamine neuron bursting, and rescues sucrose self-administration after stress [59].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [59] Scheggi S, Melis M, De Felice M, Aroni S, Muntoni AL, Pelliccia T, et al. PPARα modulation of mesolimbic dopamine transmission rescues depression-related behaviors. Neuropharmacology. 2016;110:251–9. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Peroxisome proliferator-activated receptor α (PPARα) signaling increases β2-nAChR phosphorylation, which subsequently decreases VTA dopamine neuron firing [58].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Ventral tegmental area
What the sources say
- Not checked yetcites [58] Melis M, Carta S, Fattore L, Tolu S, Yasar S, Goldberg SR, et al. Peroxisome proliferator-activated receptors-alpha modulate dopamine cell activity through nicotinic receptors. Biol Psychiatry. 2010;68:256–64. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“β-Cat regulates Dicer1, a microRNA regulator that, in turn, modulates other known pro-susceptibility genes such as Arc and Npas4 [127].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [127] Dias C, Feng J, Sun H, Shao NY, Mazei-Robison MS, Damez-Werno D, et al. β-catenin mediates stress resilience through Dicer1/microRNA regulation. Nature. 2014;516:51–5. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“FNDC5 induces thermogenesis and elevates mitochondrial gene expression [131], and resilient mice have increased NAc metabolism [132].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [131] Boström P, Wu J, Jedrychowski MP, Korde A, Ye L, Lo JC, et al. A PGC1-α-dependent myokine that drives brown-fat-like development of white fat and thermogenesis. Nature. 2012;481:463–8. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In both male and female mice, NAc ERα overexpression increases sucrose preference and promotes CSDS-resilience in males [133].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [133] Lorsch ZS, Loh Y-HE, Purushothaman I, Walker DM, Parise EM, Salery M, et al. Estrogen receptor α drives pro-resilient transcription in mouse models of depression. Nat Commun. 2018;9:1116. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Egr3 is upregulated specifically in D1-MSNs of susceptible mice and its knockdown can prevent altered synaptic activity and stress susceptibility [88].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [88] Francis TC, Chandra R, Gaynor A, Konkalmatt P, Metzbower SR, Evans B, et al. Molecular basis of dendritic atrophy and activity in stress susceptibility. Mol Psychiatry. 2017;22:1512–9. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Social defeat increases NAc PGC1α and its downstream myokine FNDC5, and FNDC5 is upregulated more in resilient mice [130].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [130] Zhan G, Huang N, Li S, Hua D, Zhang J, Fang X, et al. PGC-1α–FNDC5–BDNF signaling pathway in skeletal muscle confers resilience to stress in mice subjected to chronic social defeat. Psychopharmacology (Berl). 2018;235:3351–8. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“RhoA is transcriptionally regulated by Egr3 [88] and in stress-naive mice, increased RhoA in D1-MSNs decreases sucrose preference in males, grooming behavior in females, and forced-swim immobility.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [138] Fox ME, Chandra R, Menken MS, Larkin EJ, Nam H, Engeln M, et al. Dendritic remodeling of D1 neurons by RhoA/Rho-kinase mediates depression-like behavior. Mol Psychiatry. 2018. https://doi.org/10.1038/s41380-018-0211-5 . [Epub ahead of print]. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Intra-NAc HDAC inhibition reverses social avoidance induced by CSDS, likely caused by increased Rac1 expression [141].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [141] Golden SA, Christoffel DJ, Heshmati M, Hodes GE, Magida J, Davis K, et al. Epigenetic regulation of RAC1 induces synaptic remodeling in stress disorders and depression. Nat Med. 2013;19:337–44. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Repressive histone modifications are both up-and downregulated after social defeat stress, and these changes are linked to genes with known roles in CSDS-susceptibility.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [140] Covington HE, Maze I, Sun H, Bomze HM, DeMaio KD, Wu EY, et al. A role for repressive histone methylation in cocaine-Iinduced vulnerability to stress. Neuron. 2011;71:656–70. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Subchronic stress also upregulates NAc Dnmt3a, but to a greater extent in stressed females.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [144] Hodes GE, Pfau ML, Purushothaman I, Ahn HF, Golden SA, Christoffel DJ, et al. Sex differences in nucleus accumbens transcriptome profiles associated with susceptibility versus resilience to subchronic variable stress. J Neurosci. 2015;35:16362–76. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“G9a overexpression promotes resilience, thought to occur by normalization of TrkB-CREB signaling [140].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [140] Covington HE, Maze I, Sun H, Bomze HM, DeMaio KD, Wu EY, et al. A role for repressive histone methylation in cocaine-Iinduced vulnerability to stress. Neuron. 2011;71:656–70. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Expression of activity-dependent histone variant H3.3 (H3f3b) is increased in the NAc in postmortem MDD tissue, after early life stress, and in CSDS-susceptible mice, an effect prevented in mice by environmental enrichment [146].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [146] Lepack AE, Bagot RC, Peña CJ, Loh Y-HE, Farrelly LA, Lu Y, et al. Aberrant H3.3 dynamics in NAc promote vulnerability to depressive-like behavior. Proc Natl Acad Sci USA. 2016;113:12562–7. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Postmortem MDD brain tissue gene expression changes reflect antemortem MDD pathophysiology.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
None of the sources cited for this claim have been checked yet.
In the paper
“Pro-susceptibility Dnmt3a overexpression [143] or constitutively active IκB kinase (IKK) [156, 157] both increase MSN spine density.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [143] LaPlant Q, Vialou V, Covington HE, Dumitriu D, Feng J, Warren BL, et al. Dnmt3a regulates emotional behavior and spine plasticity in the nucleus accumbens. Nat Neurosci. 2010;13:1137–43. source
- Not checked yetcites [156] Christoffel DJ, Golden SA, Dumitriu D, Robison AJ, Janssen WG, Ahn HF, et al. IκB kinase regulates social defeat stress-induced synaptic and behavioral plasticity. J Neurosci. 2011;31:314–21. source
- Not checked yetcites [157] Christoffel DJ, Golden SA, Heshmati M, Graham A, Birnbaum S, Neve RL, et al. Effects of inhibitor of κB kinase activity in the nucleus accumbens on emotional behavior. Neuropsychopharmacology. 2012;37:2615–23. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Histone acetylation on the Fosb promotor drives resilience in D1-MSNs, but susceptibility in D2-MSNs [124].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [124] Hamilton PJ, Burek DJ, Lombroso SI, Neve RL, Robison AJ, Nestler EJ, et al. Cell-type-specific epigenetic editing at the Fosb gene controls susceptibility to social defeat stress. Neuropsychopharmacology. 2018;43:272–84. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“In contrast, CUS increases dendritic length of NAc core MSNs, which is reversed by imipramine or fluoxetine treatment [154].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [154] Bessa JM, Morais M, Marques F, Pinto L, Palha JA, Almeida OFX, et al. Stress-induced anhedonia is associated with hypertrophy of medium spiny neurons of the nucleus accumbens. Transl Psychiatry. 2013;3:e266–e266. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
None of the sources cited for this claim have been checked yet.
In the paper
“Reduced dendritic complexity largely agrees with changes in other brain regions [151, 152] and is associated with reduced excitatory input but increased intrinsic excitability [88, 89], which may reflect homeostatic self-tuning [153].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [88] Francis TC, Chandra R, Gaynor A, Konkalmatt P, Metzbower SR, Evans B, et al. Molecular basis of dendritic atrophy and activity in stress susceptibility. Mol Psychiatry. 2017;22:1512–9. source
- Not checked yetcites [89] Francis TC, Gaynor A, Chandra R, Fox ME, Lobo MK. The selective RhoA inhibitor Rhosin promotes stress resiliency through enhancing D1-MSN plasticity and reducing hyperexcitability. Biol Psychiatry. 2019. https://doi.org/10.1016/j.biopsych.2019.02.007 . source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CSDS-susceptible mice upregulate cytokines IL-1β and CXCL1, and have more circulating leukocytes [175].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [175] Hodes GE, Pfau ML, Leboeuf M, Golden SA, Christoffel DJ, Bregman D, et al. Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress. Proc Natl Acad Sci USA. 2014;111:16136–41. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
None of the sources cited for this claim have been checked yet.
In the paper
“Mice lacking p11 [162], p11 reductions in NAc [163], or p11 knockout in NAc ChIs [158] is sufficient to reduce sucrose preference and increase forced-swim immobility (Fig. 2, top).”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [162] Svenningsson P, Chergui K, Rachleff I, Flajolet M, Zhang X, El Yacoubi M, et al. Alterations in 5-HT1B receptor function by p11 in depression-like states. Science. 2006;311:77–80. source
- Not checked yetcites [163] Alexander B, Warner-Schmidt J, Eriksson T, Tamminga C, Arango-Llievano M, Ghose S, et al. Reversal of depressed behaviors in mice by p11 gene therapy in the nucleus accumbens. Sci Transl Med. 2010;2:54ra76–54ra76. source
- Not checked yetcites [158] Warner-Schmidt JL, Schmidt EF, Marshall JJ, Rubin AJ, Arango-Lievano M, Kaplitt MG, et al. Cholinergic interneurons in the nucleus accumbens regulate depression-like behavior. Proc Natl Acad Sci USA. 2012;109:11360–5. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Silencing NAc cholinergic interneurons (ChIs) results in anhedonia and increases immobility in the forced-swim and tail-suspension tests [158].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Nucleus accumbens
What the sources say
- Not checked yetcites [158] Warner-Schmidt JL, Schmidt EF, Marshall JJ, Rubin AJ, Arango-Lievano M, Kaplitt MG, et al. Cholinergic interneurons in the nucleus accumbens regulate depression-like behavior. Proc Natl Acad Sci USA. 2012;109:11360–5. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“IL-6 drives production of inflammatory T-helper 17 (Th17) cells, which promote learned helplessness and social avoidance, and mice unable to produce Th17 are resilient to learned helplessness [178].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [178] Beurel E, Harrington LE, Jope RS. Inflammatory T helper 17 cells promote depression-like behavior in mice. Biol Psychiatry. 2013;73:622–30. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
None of the sources cited for this claim have been checked yet.
In the paper
“At least 40% of cells in the rodent [171] and human [172] brain are non-neuronal, but how non-neuronal cells interact with reward circuitry in MDD is unknown.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [171] Herculano-Houzel S, Lent R. Isotropic fractionator: a simple, rapid method for the quantification of total cell and neuron numbers in the brain. J Neurosci. 2005;25:2518–21. source
- Not checked yetcites [172] von Bartheld CS, Bahney J, Herculano-Houzel S. The search for true numbers of neurons and glial cells in the human brain: a review of 150 years of cell counting. J Comp Neurol. 2016;524:3865–95. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Microglia found in healthy reward circuitry are incredibly diverse [196] and more work is needed to profile their function in pathologic states.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [196] De Biase LM, Schuebel KE, Fusfeld ZH, Jair K, Hawes IA, Cimbro R, et al. Local cues establish and maintain region-specific phenotypes of basal ganglia microglia. Neuron. 2017;95:341–.e6. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Microglia in CUS mice have enhanced colony stimulating factor 1 receptor expression and enhanced phagocytotic activity, paralleled by CSF1 elevations in postmortem MDD tissue [185].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [185] Wohleb ES, Terwilliger R, Duman CH, Duman RS. Stress-induced neuronal colony stimulating factor 1 provokes microglia-mediated neuronal remodeling and depressive-like behavior. Biol Psychiatry. 2018;83:38–49. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Postmortem MDD brain tissue gene expression changes reflect antemortem MDD pathophysiology.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Bacteria in the gastrointestinal tract directly influence neural activity through sensory neurons, or by modulating the function of the hypothalamic–pituitary–adrenal axis (reviewed in ref. [197]).”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [197] Foster JA, McVey Neufeld K-A. Gut–brain axis: how the microbiome influences anxiety and depression. Trends Neurosci. 2013;36:305–12. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In the absence of stress, constitutively active IKK increases thin spine density, increases forced-swim immobility, and decreases sucrose preference after acute stress [156, 157].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [156] Christoffel DJ, Golden SA, Dumitriu D, Robison AJ, Janssen WG, Ahn HF, et al. IκB kinase regulates social defeat stress-induced synaptic and behavioral plasticity. J Neurosci. 2011;31:314–21. source
- Not checked yetcites [157] Christoffel DJ, Golden SA, Heshmati M, Graham A, Birnbaum S, Neve RL, et al. Effects of inhibitor of κB kinase activity in the nucleus accumbens on emotional behavior. Neuropsychopharmacology. 2012;37:2615–23. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
None of the sources cited for this claim have been checked yet.
In the paper
“CSDS increases IKK and NF-κB, along with the number of immature dendritic spines in the NAc of susceptible mice [156, 157].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [156] Christoffel DJ, Golden SA, Dumitriu D, Robison AJ, Janssen WG, Ahn HF, et al. IκB kinase regulates social defeat stress-induced synaptic and behavioral plasticity. J Neurosci. 2011;31:314–21. source
- Not checked yetcites [157] Christoffel DJ, Golden SA, Heshmati M, Graham A, Birnbaum S, Neve RL, et al. Effects of inhibitor of κB kinase activity in the nucleus accumbens on emotional behavior. Neuropsychopharmacology. 2012;37:2615–23. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“When lymphocytes from socially defeated mice are transplanted into Rag2−/− lymphopoenic mice, recipient mice exhibit more social interaction and less tail-suspension immobility [193].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [193] Brachman RA, Lehmann ML, Maric D, Herkenham M. Lymphocytes from chronically stressed mice confer antidepressant-like effects to naive mice. J Neurosci. 2015;35:1530–8. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Mice that lack microglial autophagy-related protein 7 exhibit impaired social interaction and increased immature synapses [194].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [194] Kim H-J, Cho M-H, Shim WH, Kim JK, Jeon E-Y, Kim D-H, et al. Deficient autophagy in microglia impairs synaptic pruning and causes social behavioral defects. Mol Psychiatry. 2017;22:1576–84. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Microglia from socially defeated mice have an increased inflammatory profile and produce more IL-6 after lipopolysaccharide (LPS) stimulation [191], similar to enhanced IL-6 release from the peripheral leukocytes of stressed mice [175].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [191] Wohleb ES, Hanke ML, Corona AW, Powell ND, Stiner LM, Bailey MT, et al. β-Adrenergic receptor antagonism prevents anxiety-like behavior and microglial reactivity induced by repeated social defeat. J Neurosci. 2011;31:6277–88. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Ccl2 reduction with short hairpin RNA restores sucrose preference and increases swimming in the forced-swim test [192].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [192] Wu X-B, Jing P-B, Zhang Z-J, Cao D-L, Gao M-H, Jiang B-C, et al. Chemokine receptor CCR2 contributes to neuropathic pain and the associated depression via increasing NR2B-mediated currents in both D1 and D2 dopamine receptor-containing medium spiny neurons in the nucleus accumbens shell. Neuropsychopharmacology. 2018;43:2320–30. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Viral knockdown of neuronal Csf1 attenuates dendritic spine pruning on mPFC neurons and prevents stress-induced anhedonia and forced-swim immobility [185].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [185] Wohleb ES, Terwilliger R, Duman CH, Duman RS. Stress-induced neuronal colony stimulating factor 1 provokes microglia-mediated neuronal remodeling and depressive-like behavior. Biol Psychiatry. 2018;83:38–49. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Similarly, although we know changes to NAc D1-and D2-MSN function are bidirectional, most of this work was done solely in male rodents.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Concluding remarks
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Mice with reduced glutamate transporter GLT-1 expression in habenular astrocytes are more stress-susceptible and exhibit increased tail-suspension immobility at baseline [200], in agreement with reduced glutamate transporter expression in learned helpless rats [201].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [200] Cui W, Mizukami H, Yanagisawa M, Aida T, Nomura M, Isomura Y, et al. Glial dysfunction in the mouse habenula causes depressive-like behaviors and sleep disturbance. J Neurosci. 2014;34:16273–85. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“The gut microbiome controls gut permeability and inflammation, and may thus participate in the neuroimmune mechanisms of depression [197].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [197] Foster JA, McVey Neufeld K-A. Gut–brain axis: how the microbiome influences anxiety and depression. Trends Neurosci. 2013;36:305–12. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These studies have revealed important adaptations in both dopaminergic and glutamatergic function within the VTA and NAc, and notably these adaptations can differ in directionality based on cell type or stress paradigm.”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Concluding remarks
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
In the paper
“Recent work indicates gut microbiota can also influence neural metabolism [198].”
§ The molecular and cellular mechanisms of depression: a focus on reward circuitry > Introduction > Non-neuronal cell types in reward circuitry
What the sources say
- Not checked yetcites [198] Zheng P, Zeng B, Zhou C, Liu M, Fang Z, Xu X, et al. Gut microbiome remodeling induces depressive-like behaviors through a pathway mediated by the host’s metabolism. Mol Psychiatry. 2016;21:786–96. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Altered reward circuit function underlies the loss of pleasure and amotivational syndrome experienced by most major depressive disorder patients.
“Altered reward circuit function is theorized to underlie the loss of pleasure and amotivational syndrome experienced by most MDD patients”
The paper relies on this without support.
Preclinical rodent models are useful for identifying cell-type-specific mechanisms that are otherwise inaccessible in human studies.
“Preclinical rodent models for studying depression have been useful for identifying the cell-type-specific mechanisms that are otherwise inaccessible in human studies.”
The paper relies on this without support.
Rats and mice do not likely experience the complex cognitive aspects of clinical depression.
“Although rats and mice do not likely experience the complex cognitive aspects of clinical depression”
The paper relies on this without support.
Rodents, similar to humans, want to work for rewards such as food, sex, and social interaction.
“rodents, similar to humans, want to work for rewards such as food, sex, and social interaction.”
The paper relies on this without support.
The stressful experiences that precipitate major depressive disorder likely represent a combination of physical and psychosocial stressors.
“the stressful experiences that precipitate MDD likely represent a combination thereof.”
The paper relies on this without support.
Postmortem MDD brain tissue gene expression changes reflect antemortem MDD pathophysiology.
“Much of the validation of the molecular changes found in rodents relies on tissue collected from postmortem MDD brains.”
The paper relies on this without support.
Rodent chronic stress models such as CSDS and CUS produce depressive-like states relevant to human MDD.
“Together, these studies provide insight into how stress exposure alters NAc MSN physiology to elicit depressive behavior.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“A number of studies have found that chronic stressors cause maladaptive adaptations in the mesolimbic DA system [148], the details of which seem to be influenced by the nature and the degree of the stressor.”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [148]
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Metadata
- Authors
- Fox, M. E., & Lobo, M. K.
- Affiliations
- University of Maryland, Baltimore (US)
- Corresponding author
- Lobo, Mary Kay
- Venue
- Molecular Psychiatry
- Published
- 2019-04-09
- Volume
- 24
- Issue
- 12
- Pages
- 1798-1815
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC6785351
- OpenAlex
- W2937907669
- Cited by
- 232
- References
- 209
- Citations by year
- 2026: 19 · 2025: 41 · 2024: 37 · 2023: 41 · 2022: 40 · 2021: 38 · 2020: 13 · 2019: 2
- FWCI
- 3.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (R01MH106500, F32 MH116574)
- U.S. Department of Health & Human Services | NIH | National Institute on Drug Abuse (R01DA038613, R01DA047843)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- depression, reward systems, anhedonia, social withdrawal, neurovegetative symptoms, weight loss, neurophysiological mechanisms, rodent models of depression
- MeSH terms
- Animals, Depression, Major Depressive Disorder, Disease Models, Animal, Humans, Motivation, Reward, Social Behavior, Weight Loss, Anhedonia
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