Evidence map›Paper›PMID 32572589›Full record

ArticlePsychopharmacology2020

Mechanisms underlying remediation of depression-associated anxiety by chronic N-acetyl cysteine treatment.

Suwarna Chakraborty, Sunil Jamuna Tripathi, T R Raju, B S Shankaranarayana Rao

Abstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  9. Article
  10. Role of Imaging Modalities andACS chemical neuroscience · 2023
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  11. Antidepressant-like Effects ofBehavioral sciences (Basel, Switzerland) · 2022
    Article
  12. Review
  13. Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Suwarna ChakrabortyDepartment of Neurophysiology, National Institute of Mental Health and Neuro Sciences (NIMHANS), Hosur Road, Bengaluru, 560 029, India.ORCID https://orcid.org/0000-0001-9456-4322
Sunil Jamuna TripathiDepartment of Neurophysiology, National Institute of Mental Health and Neuro Sciences (NIMHANS), Hosur Road, Bengaluru, 560 029, India.ORCID https://orcid.org/0000-0001-9107-2437
T R RajuDepartment of Neurophysiology, National Institute of Mental Health and Neuro Sciences (NIMHANS), Hosur Road, Bengaluru, 560 029, India.ORCID https://orcid.org/0000-0002-7742-4050
B S Shankaranarayana RaoDepartment of Neurophysiology, National Institute of Mental Health and Neuro Sciences (NIMHANS), Hosur Road, Bengaluru, 560 029, India. bssrao@nimhans.ac.in.ORCID https://orcid.org/0000-0002-8323-8211
National Institute of Mental Health and Neurosciences · IN

Funding

Indian Council of Medical Research 3/1/2/74/Neuro/2018-NCD-IIndian Council of Medical Research 45/04/2018-ANA-BMS
6 · The paper itself

Abstract

rationaleAnxiety is one of the most comorbid conditions with major depressive disorder (MDD). Depression-associated anxiety often stems from the dysfunctional hypothalamic-pituitary-adrenal (HPA) axis and its altered regulation by the amygdala. Furthermore, MDD is associated with altered glutamatergic processing leading to anxiety and impaired regulation of the HPA axis. Recent studies have demonstrated that N-acetyl cysteine (NAC), a pleiotropic drug, exerts antidepressant-like effect by modulation of hippocampal functions, periterminal release of glutamate, and/or redox systems. However, the effects of NAC on depression-associated anxiety, HPA axis hyperactivity, and amygdalar dysfunctions are relatively unknown.

objectivesAccordingly, we evaluated the effect of NAC on neonatal clomipramine (CLI)-induced adulthood anxiety and accompanying changes in plasma corticosterone levels, amygdalar volumes, neuronal/glial densities, levels of monoamines, and their metabolites in the amygdalar complex.

resultsWe found that chronic treatment with NAC reverses CLI-induced anhedonia and enhanced anxiety. Interestingly, attenuation of CLI-associated anxiety in NAC-treated rats were accompanied by a reversal of adrenal and spleen hypertrophy, and normalization of enhanced plasma corticosterone levels, indicating improved HPA axis functioning. Furthermore, NAC treatment was sufficient to reverse volumetric hypertrophy of basolateral amygdala (BLA), and altered noradrenaline (NA) metabolism in the amygdalar complex. The effects of NAC in the reversal of CLI-induced impairments were similar to that of fluoxetine (FLX).

conclusionsWe suggest that beneficial effects of NAC on antidepressive- and antianxiety-like behaviors are at least in part mediated via restoration of amygdalar and HPA axis functioning. Our results support the hypothesis that NAC might be evolved as a therapeutic strategy for reversal of amygdalar dysfunction in depression.

Indexed as

AcetylcysteineAmygdalaAnimalsAnti-Anxiety AgentsAntidepressive AgentsAnxietyCorticosteroneDepressionDrug Administration ScheduleFree Radical ScavengersHippocampusHypothalamo-Hypophyseal SystemMalePituitary-Adrenal SystemRandom AllocationRatsAcetylcysteineAnti-Anxiety AgentsAntidepressive AgentsCorticosteroneFree Radical ScavengersAnxietyBasolateral amygdalar hypertrophyDepressionHypothalamic-pituitary-adrenal (HPA) axis dysfunctionsN-acetyl cysteine (NAC)

Identifiers

PMID32572589
OpenAlexW3037083979

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.