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January 12, 2016Journal of NeuroscienceOpen Access

Myocardial Infarction Causes Transient Cholinergic Transdifferentiation of Cardiac Sympathetic Nerves via gp130

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Key result

After myocardial infarction, cardiac sympathetic nerves transiently produce acetylcholine via a gp130-dependent mechanism, which blunts norepinephrine-stimulated adaptation to high heart rates.

Population

WT C57BL/6J mice, gp130 DBH-Cre/lox mice, DBH-CreERT2 mice, ChAT lox/lox mice and male New Zealand White…

Comparison

Myocardial infarction and ex vivo application of… vs Sham-operated animals.

Design

Preclinical

Follow-up

21 days

Authors

AOAntoinette OlivasRGRyan T. GardnerLWLianguo Wang

Discussion

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Overview

May underlie post-MI chronotropic impairment; leaves open gp130 as a therapeutic target pending human studies.

Structured PICO

P
Population
Male and female mice (12-18 weeks old) and male New Zealand White rabbits used in an experimental model of myocardial ischemia-reperfusion to study autonomic nerve plasticity.
I
Intervention
Myocardial infarction (ischemia-reperfusion via 45-min LAD ligation) and ex vivo application of norepinephrine and acetylcholine.
C
Comparator
Sham-operated animals.
O
Outcome
Cardiac acetylcholine and norepinephrine levels, cholinergic gene expression in stellate ganglia, and ex vivo cardiac action potential duration and calcium transients.surrogate

Myocardial infarction induces a transient, gp130-dependent cholinergic transdifferentiation of cardiac sympathetic nerves, which may impair adaptation to high heart rates and increase arrhythmia susceptibility.

Limitations

  • Animal model findings may not fully translate to human pathophysiology.
  • Exact in vivo levels of ACh may be underestimated due to acetylcholinesterase degradation during tissue processing.

Cite This Study

Olivas et al. (2016) studied Myocardial Infarction. Myocardial ischemia-reperfusion vs. Sham surgery was evaluated on Cardiac acetylcholine (ACh) content and cholinergic gene expression. After myocardial infarction, cardiac sympathetic nerves transiently produce acetylcholine via a gp130-dependent mechanism, which blunts norepinephrine-stimulated adaptation to high heart rates.

synapsesocial.com/papers/6a6f5af178a11c550e090ceehttps://doi.org/10.1523/jneurosci.3556-15.2016
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Cardiac sympathetic nerve transdifferentiation reduces action potential heterogeneity after myocardial infarction2020 · 39 citations
  2. 2Infarction alters both the distribution and noradrenergic properties of cardiac sympathetic neurons2004 · 107 citations
  3. 3Vagosympathetic interactions in ischemia-induced myocardial norepinephrine and acetylcholine release2001 · 22 citations
  4. 4Peripheral cardiac sympathetic hyperactivity in cardiovascular disease: role of neuropeptides2013 · 65 citations
  5. 5A Non-Neuronal Cardiac Cholinergic System Plays a Protective Role in Myocardium Salvage during Ischemic Insults2012 · 66 citations