Evidence map›Paper›PMID 25765732›Full record

ArticleStress (Amsterdam, Netherlands)2015

Role of nucleus of the solitary tract noradrenergic neurons in post-stress cardiovascular and hormonal control in male rats.

Jana Bundzikova-Osacka, Sriparna Ghosal, Benjamin A Packard, Yvonne M Ulrich-Lai, James P Herman

Abstract read
In one paragraph

Article in Stress (Amsterdam, Netherlands), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Review
  2. Metabolism-Mediated Regulation of Brain-Heart Interactions.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Noradrenaline Regulation of Brain-Body Communication.Advances in experimental medicine and biology · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

5 authors.

Jana Bundzikova-OsackaDepartment of Psychiatry and Behavioral Neuroscience, University of Cincinnati Metabolic Diseases Institute , Cincinnati, OH , USA and.
Sriparna Ghosal
Benjamin A Packard
Yvonne M Ulrich-Lai
James P Herman

Funding

Brainstem Mechanisms of Stress RegulationR01MH069860 · NIMH · UNIVERSITY OF CINCINNATI · PI HERMAN, JAMES P · 2004 to 2014
$3.5M
NIMH NIH HHS R01 MH069860
6 · The paper itself

Abstract

Chronic stress causes hypothalamo-pituitary-adrenal (HPA) axis hyperactivity and cardiovascular dyshomeostasis. Noradrenergic (NA) neurons in the nucleus of the solitary tract (NTS) are considered to play a role in these changes. In this study, we tested the hypothesis that NTS NA A2 neurons are required for cardiovascular and HPA axis responses to both acute and chronic stress. Adult male rats received bilateral microinjection into the NTS of 6-hydroxydopamine (6-OHDA) to lesion A2 neurons [cardiovascular study, n = 5; HPA study, n = 5] or vehicle [cardiovascular study, n = 6; HPA study, n = 4]. Rats were exposed to acute restraint stress followed by 14 d of chronic variable stress (CVS). On the last day of testing, rats were placed in a novel elevated plus maze (EPM) to test post-CVS stress responses. Lesions of NTS A2 neurons reduced the tachycardic response to acute restraint, confirming that A2 neurons promote sympathetic activation following acute stress. In addition, CVS increased the ratio of low-frequency to high-frequency power for heart rate variability, indicative of sympathovagal imbalance, and this effect was significantly attenuated by 6-OHDA lesion. Lesions of NTS A2 neurons reduced acute restraint-induced corticosterone secretion, but did not affect the corticosterone response to the EPM, indicating that A2 neurons promote acute HPA axis responses, but are not involved in CVS-mediated HPA axis sensitization. Collectively, these data indicate that A2 neurons promote both cardiovascular and HPA axis responses to acute stress. Moreover, A2 catecholaminergic neurons may contribute to the potentially deleterious enhancement of sympathetic drive following chronic stress.

Indexed as

Adrenergic NeuronsAnimalsCardiovascular SystemCorticosteroneHeart RateHypothalamo-Hypophyseal SystemMaleOxidopaminePituitary-Adrenal SystemRatsRats, Sprague-DawleySolitary NucleusStress, PhysiologicalStress, PsychologicalSympatholyticsCorticosteroneOxidopamineSympatholyticsAcute stresschronic variable stresscorticosteroneelevated plus mazeheart rateheart rate variability

Identifiers

PMID25765732
PMCPMC4503520

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Registered trials

None linked

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.