ArticleESC heart failure2019
Learned helplessness reveals a population at risk for depressive-like behaviour after myocardial infarction in mice.
Article in ESC heart failure, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Calcineurin signaling promotes takotsubo syndrome.Nature cardiovascular research · 2023Article
- Learned Helplessness in Renal Dialysis Patients: Concept Analysis with an Evolutionary Approach.Patient preference and adherence · 2022Review
- 5-HTT Deficiency in Male Mice Affects Healing and Behavior after Myocardial Infarction.Journal of clinical medicine · 2021Article
- Epigenetic gene expression links heart failure to memory impairment.EMBO molecular medicine · 2021Article
- Learned helplessness reveals a population at risk for depressive-like behaviour after myocardial infarction in mice.ESC heart failure · 2019Article
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Authors and funding
12 authors.
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Abstract
aimsMyocardial infarction (MI) and heart failure (HF) are risk factors for the development of depression, additionally worsening the quality of life and patient outcome. How HF causes depression and how depression promotes HF remain mechanistically unclear, which is at least partly caused by the difficulty of in vivo modelling of psychosomatic co-morbidity. We aimed to study the potential sequence of events with respect to different depression aspects upon HF. METHODS AND
resultsMale C57BL6 mice underwent MI, followed by behavioural and echocardiographic characterization. Motility, exploration, and anxiety-like behaviour were unaffected in mice after MI. We did not observe increased depressive-like behaviour in the sucrose preference, tail suspension, or Porsolt forced swim test. Mice did not display signs of learned helplessness (LH) when compared to sham. Accordingly, cluster analysis revealed only a slightly higher quota of LH in HF (38%) vs. sham mice (32%). But strikingly, three-group cluster analysis revealed an additional intermediate subpopulation at risk for LH after HF (29%). Interestingly, this population featured elevated cardiac expression of nr4a1.
conclusionsThe LH paradigm uncovered a subtle predisposition to depressive-like behaviour after MI, whereas testing for anhedonia and despair was insufficient to show a behavioural shift in mice. Therefore, we suggest an accumulating risk profile and a multiple-hits hypothesis regarding the pathogenesis of co-morbid depression after MI. Symptoms of LH may present a marker of subclinical depression after MI, the impact of which remains to be investigated. The proposed sequence of behavioural testing enables the mechanistic dissection of cardio-psychogenic signalling in the future.
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